The Coronavirus Exposed. Part 4: More Updates

I have written several articles on the coronavirus and on masks and healthcare issues. A series of links have been provided at the bottom of this article for your convenience. This article will, however address a different aspect of the virus or on healthcare issues in general.

I know COVID has been around a while, so now even my third part is acting very sluggish. So I will start a 4th part. The previous three sections will remain all accessible for viewing, though they will now function as an archive.

(Last Updated on 11/18/2023)

Table of Contents

-COVID rebounds aren’t definitively linked to Paxlovid—here’s what we know

-Doctors Sue Biden Admin, Big Tech Over COVID Censorship

-COVID-19 took a unique toll on undocumented immigrants

-What scientists have learnt from COVID lockdowns

-One of Long COVID’s Worst Symptoms Is Also Its Most Misunderstood

-Is the COVID-19 pandemic over?

-Could COVID-19 trigger depression?

-‘Speed of Science’ — A Scandal Beyond Your Wildest Nightmare

-COVID-19 can interfere with your period in many ways. Here’s how.

-COVID-19 can ruin your sleep in many different ways—here’s why

-Is COVID-19 Even Real?

-Severe COVID could cause markers of old age in the brain

-Why does COVID-19 cause brain fog? Scientists may finally have an answer.

-How do you know if you have long COVID?

-Omicron variant XBB.1.5 is the most contagious yet

-CDC Investigating Possible Link Between COVID Vaccine and Increased Risk of Stroke

-COVID-19 Leads to an Alarming Rise in Heart Attacks

-Top Expert Sounds the Alarm, Calls for Immediate Suspension of All mRNA Vaccines

-COVID drug drives viral mutations — and now some want to halt its use

-WHO abandons plans for crucial second phase of COVID-origins investigation

-COVID-origins study links raccoon dogs to Wuhan market: what scientists think

-COVID-origins data from Wuhan market published: what scientists think

-For some long COVID patients, exercise is bad medicine

-COVID’s future: mini-waves rather than seasonal surges

-WHO declares end to COVID-19’s emergency phase

-Why is COVID life-threatening for some people? Genetics study offers clues

-How COVID-19 harms the heart

-COVID cases are rising again. Here’s a refresher on everything you forgot.

-What is POTS? This strange disorder has doubled since the pandemic

-What causes long COVID? The answer might be in your gut

-Now we know how COVID attacks your heart


COVID rebounds aren’t definitively linked to Paxlovid—here’s what we know

When Anthony Fauci announced in June that he had experienced a “rebound” case of COVID-19—testing positive mere days after a negative test result—many Americans were shocked this could happen. But in the intervening weeks, a growing number of people have suffered a rebound themselves or encountered others in similar straights, including another high-profile case just last week of President Joe Biden.

“It’s hard to ignore the anecdotal evidence of rebounding peppered throughout social and mass media,” says Katelyn Jetelina, an epidemiologist at the University of Texas School of Public Health who writes the popular blog Your Local Epidemiologist.

A rebound occurs when a person tests positive for COVID-19 or suffers a recurrence of symptoms between two and eight days after recovering from the initial infection and testing negative, according to a health alert for physicians issued by the Centers for Disease Control and Prevention in May. In many cases, the rebound is happening in people taking an antiviral medication, which is recommended for individuals at high risk of progressing to a severe form of COVID-19, ending up in the hospital or dying from the infection.

Those are the known facts. Everything else about rebound is currently subject to speculation.

“There’s a lot we don’t know right now,” Jetelina says. “We don’t know how often this is happening, and we don’t know what’s causing it.” And while the phenomenon is often linked to antivirals, more than one factor may be involved.

How frequently are COVID-19 patients rebounding? 

Pfizer’s official clinical trial for its antiviral Paxlovid took place when the Delta variant was predominant in the U.S. That trial reported that fewer than 2 percent of people taking the medication—which involves two pills taken twice daily for five days—experienced rebound.

But doctors who have prescribed Paxlovid in more recent months say that figure is likely now a woeful undercount.

Scott Roberts, an infectious diseases physician at Yale Medicine, says his experience puts the number closer to 5 percent. That tracks with a study posted online but not yet peer-reviewed in which researchers from Case Western Reserve University evaluated rebound cases following courses of Paxlovid and Lagevrio—the Merck antiviral generically known as molnupiravir—between January and June 2022.

Paxlovid is the more widely prescribed antiviral, with three million courses given since its emergency authorization by the U.S. Food and Drug Administration last December. By contrast fewer than half a million courses have been administered for Lagevrio.

In the Case Western Reserve research, some 3.5 percent of Paxlovid takers rebounded after seven days; for those taking Lagevrio, the number was close to 6 percent.

With the latest Omicron variant, BA.5, dominant in the U.S. since early July, some doctors think today’s rebound numbers are not only higher but will continue to rise. Aftab Khan, an internal medicine physician in Davenport, Florida, says that about a quarter of his elderly Paxlovid patients have rebounded, and he expects a further increase because this wily subvariant is likely even better at evading antibodies.

Is rebound linked to antiviral treatment? 

Though the rate of rebounds seems to be higher in those taking antiviral medicine, there isn’t enough data to definitively say that there is a link between the two.

In the Pfizer Paxlovid trial, patients taking placebos rebounded at rates similar to those getting the drug. The CDC states that a brief return of symptoms “may be part of the natural history” of COVID-19 in some people, whether or not they’ve received an antiviral. For this reason, the CDC calls the phenomenon COVID-19 rebound rather than the more widely used term Paxlovid rebound.

But Yale’s Roberts says that while symptoms did reappear in some cases before the antivirals were authorized, this was very rare.

What causes COVID-19 to rebound is another issue that’s currently unclear. According to Jetelina, it’s possible the drug doesn’t sufficiently clear the virus in some people, so once the patient stops taking it after the fifth day, the microbe can start multiplying again.

It may also be that rebound happens when treatment is started too early; current recommendations call for initiation as soon as possible, ideally within the first five days, but that may not give the immune system time to mount a full response. It’s also possible that some people had been reinfected after their illness ended, although this wouldn’t explain rebound cases in people who hadn’t had any additional exposure after recovering.

According to Pfizer spokesperson Kit Longley, rebound is not caused by the virus becoming resistant to Paxlovid, although he notes that the company continues to monitor the data. In a report posted online in June but not yet published in a medical journal, Pfizer researchers describe details from their original study, in which rebound was not linked to any mutations occurring in the virus in people taking the drug.

This is consistent with research published in June by a team at the University of California, San Diego, School of Medicine. That team performed detailed antiviral sensitivity and neutralizing antibody testing on a single rebounding patient. They concluded the relapse was not caused by drug resistance or by impaired immunity, but instead likely resulted from the virus having insufficient exposure to the drug.

Who is at greatest risk of rebounding and what should you do?

Who might rebound—and what they should do about it—are also open questions.

In the Case Western Reserve research, people with the most serious medical conditions, such as organ transplant recipients, those on immunosuppressant medicines, those with comorbidities like heart disease or diabetes, and tobacco users were most prone to COVID-19 rebound.

Of course, this is also the group most likely to reap the benefits from taking an antiviral.

Taking an antiviral also seems to be especially important for high-risk individuals over age 65, according to an Israeli study of more than 2,000 people that has not yet been reviewed by other scientists. People in that age group treated with antiviral therapy were 67 percent less likely to be hospitalized and 81 percent less likely to die than those not taking the drug, a finding not found for the younger study subjects.

If someone does experience rebound, the CDC says they should assume they’re infectious and begin another round of five-day isolation, followed by five days of masking. However, the agency admits that no one knows yet whether a person’s infectiousness during rebound differs from that during their initial bout.

Some doctors say rebound patients can leave their homes as soon as an antigen test again comes back negative. But Yale’s Roberts thinks it’s imprudent to end isolation early no matter the test results. “Testing errors are frequent, and the lower sensitivity of rapid antigen tests would make me nervous if someone leaves isolation before the allotted time,” he says.

Fortunately, most cases of rebound have been mild. Rebound led to hospitalization in fewer than one percent of cases, according to a CDC study published in June. This makes sense, Roberts says, “since the virus is starting at a lower amount, and the initial drug course allowed time for immunity to build.”

Some doctors are prescribing a second round of Paxlovid—something Fauci says was given to him—but there is no evidence yet to support this expanded regimen. Pfizer’s Longley says the company is currently working with the U.S. Food and Drug Administration to finalize a study protocol evaluating whether this is beneficial.

It’s also possible that a longer course of the initial antiviral medication, such as seven or 10 days instead of five, might be more effective at blocking replication of the BA.5 Omicron subvariant, which generates higher viral loads than its predecessors, says Jill Weatherhead, an infectious diseases expert at Baylor College of Medicine. She notes, though, that such a protocol would need to be studied before physicians might start prescribing it.

Uncertainties surrounding rebound should not prevent people who could benefit from antivirals from taking them, Roberts insists, even though some patients have told him they want to avoid the drug for this reason.

“This is a dangerous and misguided strategy,” he says. The purpose of an antiviral is to prevent hospitalization and death, not to keep someone from needing to isolate longer.

Doctors Sue Biden Admin, Big Tech Over COVID Censorship

A group of doctors has filed a lawsuit against several big tech companies, claiming that Twitter, Google, and Facebook worked with the government to censor criticism of federal and state COVID policies in violation of the First Amendment.

The case, State of Missouri v. Joseph R. Biden, involves a group of prominent physicians and epidemiologists who were critical of the government’s restrictive COVID policies, including lockdowns, mask mandates, and vaccine mandates.   The doctors made Freedom of Information Act requests related to the White House’s public statements in 2021 about working with Big Tech to suppress COVID misinformation. As a result of those FOIA requests, they claim to have found emails and documentation that can prove that the CDC and the Department of Homeland Security asked Google, Twitter, and Facebook to take down certain social media posts and to suspend certain accounts for questioning COVID policies.   The lawsuit is arguing that at that point, these companies were no longer acting just as private entities, but as arms of the government. If true, their actions would be unconstitutional.    New Civil Liberties Alliance’s press release states in part, “This insidious censorship was the direct result of the federal government’s ongoing campaign to silence those who voice perspectives that deviate from those of the Biden Administration. Government officials’ public threats to punish social media companies that did not do their bidding demonstrate this linkage.”
Tech Response
The tech companies could deny they were acting as a result of government pressure, as part of the Communications Decency Act, known as Section 230, gives Big Tech some special protection from civil liability. Kara Frederick, director of the Tech Policy Center at the Heritage Foundation, told Morning Wire that will likely be their defense.

(Update 9/2/2022)

*Note it looks like that my Covid Vaccine article has reached a critical mass, and since the Covid related updates have slowed down substantially I will be just adding all of these updates to this posting. So the vaccine posting can now be considered to be a archived file along with the three main Covid postings as well.

COVID-19 took a unique toll on undocumented immigrants

The pandemic compounded barriers to accessing medical care—and many continue to delay or forgo treatment.

(Update 9/4/2022)

Imelda fled sexual violence at the hands of drug cartels in rural Puebla, about two hours outside of Mexico City, and arrived in New York City in 2013. She had no health insurance, barely spoke English, and as an undocumented immigrant, she avoided situations that required revealing her identity.

So in March 2020, even as the city became the national epicenter of the COVID-19 pandemic, Imelda, who asked that her surname not be used due to risk of deportation, resisted going to the hospital for her escalating fever and fatigue. “When the symptoms began, I wanted to go,” Imelda says, but her fears outweighed her desire for treatment.

Since arriving in the U.S. Imelda had visited a hospital only once, for the birth of her second daughter. But in addition to worries about revealing her immigration status, she was afraid of incurring medical bills that exceeded what she earned cleaning houses. Delaying or forgoing care for COVID-19 was a decision that Imelda and many other undocumented immigrants made due to the unique healthcare challenges they face in America—challenges of inequality that are having nationwide consequences.

The U.S. is home to more immigrants than any other country in the world: Per the latest estimates, 46.7 million foreign-born individuals reside in America, making up nearly 14 percent of the national population. About 11 million of these people are undocumented, but they’ve filled critical jobs that citizens often don’t want, including working in agricultural fields, the service industry, and in healthcare facilities, while paying billions in taxes each year.

According to a December 2020 report from the bipartisan political organization, 69 percent of undocumented immigrant workers in the U.S. held jobs that were deemed essential during the pandemic—and they were 50 percent more likely to get COVID-19 than U.S.-born workers. For many, that’s meant surviving a public health emergency while working low-paying jobs (often on the frontlines) that don’t offer benefits; it can also mean being ineligible for free or subsidized public health insurance. To compound these problems, countless workers are unaware of their coverage options or fear accessing them.

A 2017 study found that about half of the undocumented immigrants living in America lacked necessary health insurance. That often leaves a large proportion of this community delaying care, which could result in health complications or an advanced illness and a greater reliance on emergency rooms. “When they’re unable to pay those costs, the money goes into uncompensated care costs, raising the debt in the healthcare system,” says Drishti Pillai, director of immigrant health policy at the Kaiser Family Foundation, a nonprofit organization focusing on national health issues.

For those like Imelda living in the shadows, the COVID-19 pandemic once again revealed the deep-seated inequities to accessing medical care in America. Even today, people in this underserved community continue to suffer, often with little help.

Too little care, too late

In addition to medical costs and insurance access, a sustained lack of trust has dissuaded the country’s growing immigrant population from engaging with the healthcare system. This mistrust arises in part from the discrimination immigrants have experience based on how they look, where they’re from, or their inability to speak English. “It’s really hard,” Imelda says.

Anti-immigrant rhetoric has also kept the undocumented community from accessing timely care. At the Elmhurst Hospital Center in New York City, which caters largely to New York City’s low-income immigrant population, “we’ve watched our volume dip at times when there are national discussions about immigration and whether it was good or bad for the country,” says Stuart Kessler, one of the hospital’s emergency medicine physicians.

In Houston, researchers noted that Latina immigrants delayed their first prenatal care visit and reduced the number of visits overall during their pregnancies after July 2015, when rhetoric around deportation intensified in the lead-up to the 2016 presidential election.

That fear of accessing healthcare in a climate of growing anti-immigrant sentiment continued through 2020 when the COVID-19 pandemic hit and further exacerbated already existing barriers between the healthcare system and this underserved population.

“We just didn’t realize our systems of care were this fractured, and that so many people could fall through the cracks because the cracks were just so huge,” says Jairo Gúzman, president of Mexican Coalition, an advocacy group for child and family rights based in New York.

That was true for Imelda in March 2020. With no one to consult and no place to isolate, she endured her COVID-19-like symptoms for a week in the three-bedroom apartment she shared with seven others—including her husband and two kids. As she found herself struggling to breathe a hospital visit became an urgent necessity.

She went to a hospital and, at an overwhelmed emergency room, nervously waited for an online interpreter so she could talk with the medical staff and find out if she had COVID-19. “Five minutes is all I got,” she says, which wasn’t enough for her to explain all her symptoms while also answering the doctor’s questions and noting his instructions about next steps.

The medical team didn’t give her a COVID-19 test because a chest x-ray showed no irregularities. Instead a nurse gave her Tylenol to reduce her fever and, within a few hours, Imelda was sent home with the assurance that she’d receive check-in phone calls and could return if her symptoms worsened.

But no calls came, and Imelda’s health continued to deteriorate. Over the next four weeks, her breathing became increasingly difficult and her body was consumed by extreme exhaustion. “I would walk a little and I’d be gasping for breath, and on some days I couldn’t stand up at all,” she says. “I thought I was done—this was it.”

A $400 bill from her initial ER visit deterred her from seeking further care. (The hospital later reduced her bill by half because she had lost her cleaning job.)

Recalling these struggles brought Imelda to tears when we met at her home in May 2022. She is aware that the consequences of delaying care could have been fatal, and she knows others who are still batting lingering symptoms without seeking medical help.

COVID-19 hits those living in the shadows

Even now the true impact of COVID-19 on undocumented immigrants, especially in the early months of the pandemic, remains murky.

One of Susan Rodriguez’s patients in New York—an 88-year-old Ecuadorian women—lost her son to COVID-19, possibly because they waited too long to seek medical care. They were both undocumented and uninsured and decided to treat his symptoms at home. Eventually, they had no choice but to call 911 and take him to a hospital. But the medical interventions came too late. He passed away two days later, leaving his mother distraught and unsure how to cope.

“She had never sought therapy in her life,” says Rodriguez, a clinical social worker and a licensed therapist. “She came with a lot of guilt,” and wished she had known she could have applied for emergency Medicaid to cover the costs.

“We heard of cases where people stayed at home or delayed care for COVID-19 almost every day,” adds Don Garcia, medical director at Clínica Romero, a community health center in Los Angeles that primarily serves Latino and immigrant populations. Some of these people narrowly escaped death.

Antonio, who asked that his full name not be used due this immigration status, was one of them. He is undocumented and had arrived in Oxnard, a city in the Greater Los Angeles Area, from Mexico in 2019. Terrified of revealing his personal details, the 40-year-old restaurant worker remained uninsured and unvaccinated. He got infected in December during the Omicron wave and his condition deteriorated rapidly.

“By the sixth day I was so desperate that I wanted to go to a hospital,” he says, but he decided against it because of his immigration status. “There were three days when I was completely lost, barely conscious, I had no clue if I was alive,” he says, overwhelmed with emotion as he shifts in his chair and grabs a tissue to wipe away tears.

Embarrassed, Antonio apologizes and looks around the conference room at the nonprofit Mixteco Indigena Community Organization Project’s office in Oxnard in April this year. After a pause, Antonio recalls how he begged his boss to take him back after missing work for almost 22 days; he was behind on rent and had a family to support. “I think it’s very different to have COVID as an immigrant in this country,” he says.

Those who did turn to the medical system sometimes experienced discriminatory behavior in the form of being treated rudely or disrespectfully for not speaking English, or they felt that they weren’t being heard.

“People in the healthcare system can come with a biased lens,” says Mireya Vilar-Compte, a public health professor at Montclair State University in New Jersey with expertise in healthcare inequities. She stresses a need for more doctors, nurses, and administrative staff from diverse ethnic and racial backgrounds as one part of the solution.

Living with long COVID

More than two years into the pandemic, undocumented immigrant populations still feel they have few places to turn as they battle the aftereffects of the disease that disproportionately impacted them. With little help, some are enduring long COVID symptoms, including fatigue, brain fog, and breathing and sleeping difficulties, as well as anxiety and depression.

In Los Angeles, Ana, who asked that her last name not be used fearing deportation, has been self-medicating to manage the fatigue and body pain that has lingered for months after her COVID-19 infection last summer. She has been avoiding a visit to a doctor because she’s uninsured and undocumented, so the 38-year-old part-time house cleaner uses painkillers that she buys from street vendors in downtown L.A.

“It has gotten to a point where I feel depressed that I’m going to have to take these pills for life,” she says. “I need to work fast, but I do get tired.”

Fortunately for Imelda, who despite being vaccinated has contracted COVID-19 twice since her March 2020 diagnosis, New York expanded its healthcare-for-all program to her borough, Queens, in September 2020. Called NYC Care, this city-funded program guarantees low-cost and no-cost services to all New Yorkers who don’t qualify or can’t afford health insurance, irrespective of immigration status.

Since then Imelda has been seeking healthcare to cope with her heart palpitations, trouble sleeping and breathing, and post-COVID depression. She’s had MRIs, cardiac screenings, and has been seeking physical and psychotherapy.

Nationwide, though, such programs are rare, Pillai says. Today, seven states and the District of Columbia offer some type of healthcare coverage for some or all age groups of the undocumented population, but she says the effort should be expanded nationwide. When individuals can use primary and preventative care, they rely less on emergency medical services, which are extremely expensive. “Economically, in the long-term, it’s not the best idea to prevent some groups from accessing benefits to which a lot of them already contribute,” Pillai says.

But such an effort would require addressing the existing bias and discrimination in the medical system. Despite now being insured, Imelda says “I don’t feel like they see me the same way as they see someone who’s American.” Especially when it comes to healthcare, “I wish everyone was treated the same.”

What scientists have learnt from COVID lockdowns

Restrictions on social contact stemmed disease spread, but weighing up the ultimate costs and benefits of lockdown measures is a challenge.

(Update 9/7/2022)

A man walks across a deserted highway in Wuhan, China, in February 2020, during the city’s first lockdown. Credit: Getty Images

In March 2021, a doctor in Brazil named Ricardo Savaris published a now-discredited research paper that went viral on social media.

It had been a year since the first wave of the COVID-19 pandemic forced governments to apply the desperate measures collectively known as lockdowns — cancelling sporting and cultural events, closing retail outlets, restaurants, schools and universities, and ordering people to stay at home. At the time, countries were once again dialling lockdown policies up or down, as the Alpha variant of the coronavirus SARS-CoV-2 surged in different places.

Lockdown measures did what they were supposed to. When they were enforced rigorously enough to reduce people’s social contacts sharply, they shrank COVID-19 outbreaks; several studies had demonstrated this.

But Savaris, an obstetrician and gynaecologist at the Federal University of Rio Grande do Sul in Porto Alegre, tried a fresh analysis together with three colleagues (who worked in statistics, computer science and informatics). They compared 87 locations around the world, in pairs, to see whether a lower rate of COVID-19 deaths correlated with greater time spent at home, assessed using anonymized cellphone data released by Google. In most cases, their paper in Scientific Reports concluded, it didn’t.

The paper was highlighted by prominent lockdown sceptics and some news sites and swiftly gained notoriety. “The findings were quite remarkable, on the face of it,” says Gideon Meyerowitz-Katz, an epidemiologist at the University of Wollongong, Australia. As he and others would show, the results were wrong, because of errors in the paper’s choice of statistical methods.

Within a week, Scientific Reports added an ‘editor’s note’ to the paper, alerting readers to criticisms. Nine months later, the journal published two letters that laid out the paper’s errors. A week after that, it retracted the work, although neither Savaris nor his co-authors agreed with the retraction. (Scientific Reports is published by Springer Nature; Nature’s reporting is editorially independent of its publisher.)

The retracted paper is not the only one to contend that lockdowns failed to save lives. But these analyses are out of step with the majority of studies. Most scientists agree that lockdowns did curb COVID-19 deaths and that governments had little option but to restrict people’s social contacts in early 2020, to stem SARS-CoV-2’s spread and avert the collapse of health-care systems. “We needed to buy ourselves some time,” says Lauren Meyers, a biological data scientist at the University of Texas at Austin.

At the same time, it’s clear that lockdowns had huge costs, and there is debate about the utility of any subsequent lockdown measures. School and university closures disrupted education. Closing businesses contributed to financial and social hardship, mental ill health and economic downturns. “There’s costs and benefits,” says Samir Bhatt, a public-health statistician at Imperial College London and the University of Copenhagen.

Scientists have been studying the effects of lockdowns during the pandemic in the hope that their findings could inform the response to future crises. They have reached some conclusions: countries that acted quickly to bring in stringent measures did best at preserving both lives and their economies, for instance. But researchers have also encountered difficulties. Analysing competing harms and benefits often comes down not to scientific calculations, but to value judgements, such as how to weigh costs that fall on some sections of society more than others. That is what makes lockdowns so hard to study — and can lead to bitter disagreement.

Tricky calculation

There’s a fundamental difficulty with analysing the effects of COVID-19 lockdowns: it is hard to know what would have happened in their absence.

Lockdowns do reduce viral transmission, as the shutdown of Wuhan, China, showed when SARS-CoV-2 first emerged. Even in countries that didn’t emulate China’s all-in approach of closing borders, ordering citizens to stay at home and isolating people with COVID in central facilities, lockdown measures still cut disease spread. In May 2020, for instance, Bhatt and others analysed lockdowns in 11 European countries and extrapolated from the fall in viral transmission that these measures alone had saved more than 3 million lives.

That paper’s methodology has also been questioned, however. One issue is that it could have overstated the size of the benefit because it assumes that without lockdown mandates, people wouldn’t have reduced their social contacts. In reality, rising deaths would probably have changed people’s behaviour.

That happened in Florida, for instance, where data show a reduction in mobility during the first wave about two weeks before lockdowns, says health-policy researcher Thomas Tsai at the Harvard T.H. Chan School of Public Health in Boston, Massachusetts. “People were watching the news in New York and Boston and seeing how severe COVID could be,” he says.

One analysis5 by political scientist Christopher Berry and his colleagues at the University of Chicago, Illinois, supports this. It suggests that US states’ shelter-in-place orders did little to further reduce COVID-19 cases and deaths, not because social distancing doesn’t work, but because people were already avoiding contact before the orders were imposed.

Other researchers have tried instead to compare whether countries with stricter lockdown policies performed better than those with more relaxed ones on measures such as disease transmission rates or deaths. This isn’t simple, either: enforcement, levels of government aid and compliance with official policies differed from one region to another — as did cultural context and a host of other factors, including population densities, levels of social contact and viral prevalence.

Take Sweden, for instance, which imposed relatively light restrictions in early 2020, keeping schools open for all but the oldest students. It experienced a lower rate of excess deaths in 2020 than did many other western European nations. But it is also a country where many people live alone (the average household size in Sweden is the lowest in the European Union), and where people have high trust in government, making it much easier for official recommendations alone — rather than mandates — to reduce social contacts and slow disease spread. Far from carrying on life as normal, Swedes reduced their mobility, as shown by mobile-phone data. Even so, its Nordic neighbours that imposed lockdowns performed better in 2020: age-standardized mortality rates show that Denmark, Finland and Norway experienced fewer deaths than normal that year, whereas Sweden experienced slightly more than usual. (As in other countries, Sweden also failed to prevent the most vulnerable people, such as those in elder-care homes, from dying of COVID-19.)

“It wasn’t really clear what is the best way of estimating the effectiveness of [lockdown] measures,” says Peter Klimek, a data scientist at the Medical University of Vienna. Still, by tracking the stringency and timing of government policies in more than 100 countries, researchers at the University of Oxford, UK, and their colleagues did find that the more stringent a nation’s containment policies, the more successful it was at averting deaths from COVID-19.

It is even harder to tease out subtler insights, such as which of the grab bag of lockdown policies — from closing schools to ordering people to stay at home — had the most effect, especially because policies were often announced in quick succession.

After the first wave of COVID-19, Klimek’s team analysed thousands of government interventions. The group noted that some measures seemed effective according to one modelling approach, but not according to others, and that their effectiveness estimates came with wide uncertainty ranges. But the researchers were able to produce an overall ranking (see ‘How effective were COVID-19 interventions?’). The most effective measures were policies banning small gatherings and closing businesses and schools, closely followed by land-border restrictions and national lockdowns. Less-intrusive measures — such as government support for vulnerable populations, and risk-communication strategies — also had an impact. Airport health checks, however, had no discernible benefit.

Other studies have tried to put more precise figures on the effects of lockdown policies, but their findings differ. An analysis of 41 countries in Europe and elsewhere found that stay-at-home orders had a relatively small impact on transmission, reducing R — the average number of people that one person with COVID-19 will go on to infect — by just 13% beyond what could be achieved by closing schools and universities (38%) or limiting gatherings to 10 people or fewer (42%). Yet Bhatt’s analysis of 11 countries suggested that stay-at-home orders cut R by 81%, with school closures, public-event bans and other measures being less important. Klimek warns against generalizing about the effectiveness of lockdown policies on the basis of figures such as these. “The effectiveness of each intervention is highly context dependent,” he says. What several analyses suggest is that no single intervention can reduce R to below 1 (signifying that infections are declining): multiple measures achieve this by working in concert.

Go hard, go fast

The pre-vaccine period of the pandemic does show that countries that acted harshly and swiftly — the ‘go hard, go fast’ approach — often fared better than those that waited to implement lockdown policies. China’s harsh lockdowns eliminated COVID-19 locally, for a time. Successful countries that learnt from this were “proactive”, according to a May 2021 report by the Independent Panel on Pandemic Preparedness & Response, established by the World Health Organization in September 2020 to review the global response. Examples include island nations such as Iceland, Australia and New Zealand, which also benefited from being able to close their borders and take action before many people with the virus arrived.

Others have echoed this. Epidemiologist Edward Knock and other members of the Imperial College COVID-19 response team concluded that nationwide lockdown was the only measure that consistently took R below 1 in England. And the earlier that strict measures were imposed, the better. Knock estimated that had England introduced a nationwide lockdown one week earlier in March 2020, it would have halved deaths during the first wave. A study of government responses in Asia also suggested that a ‘go hard, go fast’ approach was best.

But harsher lockdowns aren’t always more effective by themselves, especially in countries where it is difficult for people to stay at home. Peru is an example. It imposed early and strict lockdown measures, but experienced an excess death rate much higher than did other countries in the region that used less draconian measures. Peru is still held up as evidence that lockdowns don’t work — but in fact it struggled to enforce them. The country has a large informal workforce, combined with expensive and inadequate health infrastructure. Despite lockdowns, many Peruvians continued to venture out to shop and to work, and so transmission remained stubbornly high, says Camila Gianella Malca, a public-policy researcher at the Pontifical Catholic University of Peru in Lima.

Second wave

The impacts of lockdowns also differed from one pandemic wave to the next. By the time second waves emerged, so much had been learnt about the virus that people’s behaviour was quite different. By October 2020, population-wide masking policies had become common. Schools and other settings established physical-distancing measures to keep people apart, and people took more precautions when local transmission increased. Hospitals also learnt quickly how best to treat COVID-19: death rates after the first wave decreased by 20% owing to improved treatment alone.

Together, these changes dampened the extent to which countries benefited from lockdowns. For example, several studies found that school closures during the first wave reduced the spread of COVID-19. Yet Bhatt’s analysis suggests that second-wave school closures had a much smaller effect. “We were surprised by that, to be honest,” he says.

Only a handful of countries continued to take a ’go hard, go fast’ approach after the first wave. Countries that had aimed for elimination — China, Australia, New Zealand and Vietnam, for example — saw that it worked and then went harder and faster, according to research by Anna Petherick, a public-policy researcher at the University of Oxford’s Blavatnik School of Government and her colleagues, who tracked government policies in more than 180 countries. But in countries where belated first-wave lockdowns had merely lessened transmission, governments became less likely to take early action, tolerating higher case numbers in subsequent waves before ordering lockdowns (see ‘Thresholds for lockdown’).

Blunt tool?

Some researchers argue that countries could have avoided blunt all-of-society lockdowns, especially after the measures taken early in 2020. Among them is Mark Woolhouse, an infectious-disease epidemiologist at the University of Edinburgh, UK, who advised the Scottish government during the pandemic. He argues that it might have been possible to avoid the closing of schools and cooping-up of younger people — who were at lower risk of COVID-19 — while focusing efforts on protecting vulnerable and older people as soon as high-risk individuals and settings were identified. “This pandemic was crying out for [a] precision public-health response, because the risks associated with the public-health threat with the virus were so focused on a small minority, and the harms done by things like lockdown were not focused on the same people,” he says.

But many researchers have pushed back against the idea that a more targeted approach was ever possible. Klimek says that roughly one-third of the population in wealthy nations was vulnerable because of underlying health conditions, so targeted measures would have been difficult to implement. And the virus has caused not only deaths but also post-infection illnesses such as long COVID — which has emerged as a health burden even for people who had mild disease.

Another targeted option for governments considering how to reopen societies might have been to keep only high-risk locations closed — restaurants and bars, say, or even neighbourhoods with high population mobility, says Serina Chang at Stanford University in California, who worked with colleagues to identify such places using cellphone data. But shutting down neighbourhoods would probably disproportionately affect socially disadvantaged communities. “Fairness is such an important question here,” she says.

Benefits versus harms

Woolhouse says there was scant effort to debate the scale of potential harms caused by lockdowns, meaning that policymakers were unable to weigh up costs and benefits properly. Indeed, early on, many countries adopted a ‘save lives at any cost’ approach, he says.

And lockdown policies did bring costs. Although they delayed outbreaks, saving lives by allowing countries to hang on for vaccines and drugs, they also brought significant social isolation and associated mental-health problems, rising rates of domestic violence and violence against women, cancelled medical appointments and disruption to education for children and university students. And they were often (although not always) accompanied by economic downturns.

But the common refrain that lockdowns involved a choice — saving lives versus livelihoods, or lives versus the economy — is a false dichotomy, says Stuart McDonald, an actuary and founder of the UK-based COVID-19 Actuaries Response Group, a community of specialists who have carried out regular analyses of mortality during the pandemic. If the UK government had not imposed belated lockdowns in 2020, hospital systems would have been overrun, death rates for all kinds of illnesses would have rocketed and economies and livelihoods would have collapsed anyway, he says. One analysis15 up to November 2021 estimated that the United States lost US$65.3 billion a month during lockdowns. But another16 estimated that US lockdowns from early March until the end of July 2020 added between $632.5 billion and $765 billion to the economy, compared with the alternative of no lockdowns. Unsurprisingly, the countries that did best in terms of saving lives and protecting the economy were those that acted fast with strict lockdowns.

What is more, some governments did at least try to consider various harms, McDonald says. In July 2020, for instance, McDonald attended a meeting of the UK government’s COVID-19 advisory group to discuss efforts to model the direct and indirect health impacts of lockdowns, measured by the preservation or loss of quality-adjusted life years — QALYs. (This measure gives more weight to younger lives than the lives of older people, who are judged to have lost fewer QALYs if they die.) Fewer deaths from road accidents were tallied as a benefit of lockdown, for instance; QALYs lost owing to delayed cancer diagnoses, or poorer health owing to loss of income, were harms. In August 2020, the report discussed at the meeting was publicly released: it argued that QALYs lost would have been three times higher had there been no mitigation measures, such as lockdowns, in place. (McDonald was not involved in writing it, but contributed to subsequent versions of the report.)

Not all harms can be accounted for in this way. Loss of education because of school closures might indirectly harm children in the long run, potentially decreasing their future earnings and placing them at greater risk of poorer health outcomes. McDonald says that such harms are so far off — decades, in some cases — that they can’t readily be factored into a QALY ledger.

Value judgements

Pure economic analyses of whether lockdowns were worth it generally try to estimate the value of lives saved and compare that with the costs of economic downturns. But there is no consensus on how to make this comparison. Tweaks to the value placed on human life in these analyses can alter conclusions about whether lockdowns were worth it, found Lisa Robinson, a public-policy analyst at the Harvard T.H. Chan School of Public Health, and her colleagues. If older lives are assigned a lower monetary value than younger ones, for instance, then — because COVID-19 disproportionately affected older people — lockdowns might be judged to have provided less benefit than if all lives are valued equally.

Jonathan Aldred, an economist at the University of Cambridge, UK, says that cost–benefit calculations of this kind are ill-suited to decision-making during an emergency, given the numerous sources of uncertainty. Putting monetary values on everything — from lives lost to the economic hit caused by shop closures — can give the impression that decisions about lockdowns are objective. But, says Aldred, the upshot is that “you’re hiding the fact that there are ethical judgements that have been made”. Policymakers should instead have a transparent discussion about the ethics of weighing costs and benefits, says Aldred, rather than suggest there is a ‘scientific’ answer. Without this kind of reckoning, we could be “back to square one” in a future pandemic, he says, with the same contentious debates about whether to close schools and at what harm to other sections of society.

The next pandemic

Now that COVID-19 vaccines and treatments for severe disease are widely available, most countries that have taken full advantage of them are unlikely to return to lockdowns. So what have researchers learnt that can inform decisions when another viral pandemic arrives?

One lesson that Klimek takes from lockdown studies is that there was an early window of opportunity when the virus could have been eliminated — as it was, in effect, in countries such as China, Australia and New Zealand. Had harsher measures been adopted sooner, and more widely, the pandemic might have played out very differently. “I think this is the big learning that we need to take away,” he says.

The paradox is that a successful early clampdown, or hard and fast action against a virus that turns out to be milder than initial indications suggest, could lead to complaints of overreaction.

A future threat might, of course, also spread in a completely different way from COVID-19. Ethical choices could look very different if the next pandemic is caused by an influenza virus that predominantly affects and is spread by young children.

Lockdowns hold another clear lesson: they exacerbate inequalities that already exist in society. Those already living in poverty and insecurity are hit hardest. Guarding against these unequal impacts requires improved health access and financial safeguards when times are good.

And transparency is key, too: the public needs to know more about how pandemic-control policies are decided, says Tsai. “That makes public-health policymaking seem less capricious,” he says, “because it’s reactive to both the science and values.”

One of Long COVID’s Worst Symptoms Is Also Its Most Misunderstood

Brain fog isn’t like a hangover or depression. It’s a disorder of executive function that makes basic cognitive tasks absurdly hard.

(Update 9/22/2022)

On March 25, 2020, Hannah Davis was texting with two friends when she realized that she couldn’t understand one of their messages. In hindsight, that was the first sign that she had COVID-19. It was also her first experience with the phenomenon known as “brain fog,” and the moment when her old life contracted into her current one. She once worked in artificial intelligence and analyzed complex systems without hesitation, but now “runs into a mental wall” when faced with tasks as simple as filling out forms. Her memory, once vivid, feels frayed and fleeting. Former mundanities—buying food, making meals, cleaning up—can be agonizingly difficult. Her inner world—what she calls “the extras of thinking, like daydreaming, making plans, imagining”—is gone. The fog “is so encompassing,” she told me, “it affects every area of my life.” For more than 900 days, while other long-COVID symptoms have waxed and waned, her brain fog has never really lifted.

Of long COVID’s many possible symptoms, brain fog “is by far one of the most disabling and destructive,” Emma Ladds, a primary-care specialist from the University of Oxford, told me. It’s also among the most misunderstood. It wasn’t even included in the list of possible COVID symptoms when the coronavirus pandemic first began. But 20 to 30 percent of patients report brain fog three months after their initial infection, as do 65 to 85 percent of the long-haulers who stay sick for much longer. It can afflict people who were never ill enough to need a ventilator—or any hospital care. And it can affect young people in the prime of their mental lives.

Long-haulers with brain fog say that it’s like none of the things that people—including many medical professionals—jeeringly compare it to. It is more profound than the clouded thinking that accompanies hangovers, stress, or fatigue. For Davis, it has been distinct from and worse than her experience with ADHD. It is not psychosomatic, and involves real changes to the structure and chemistry of the brain. It is not a mood disorder: “If anyone is saying that this is due to depression and anxiety, they have no basis for that, and data suggest it might be the other direction,” Joanna Hellmuth, a neurologist at UC San Francisco, told me.

And despite its nebulous name, brain fog is not an umbrella term for every possible mental problem. At its core, Hellmuth said, it is almost always a disorder of “executive function”—the set of mental abilities that includes focusing attention, holding information in mind, and blocking out distractions. These skills are so foundational that when they crumble, much of a person’s cognitive edifice collapses. Anything involving concentration, multitasking, and planning—that is, almost everything important—becomes absurdly arduous. “It raises what are unconscious processes for healthy people to the level of conscious decision making,” Fiona Robertson, a writer based in Aberdeen, Scotland, told me.

For example, Robertson’s brain often loses focus mid-sentence, leading to what she jokingly calls “so-yeah syndrome”: “I forget what I’m saying, tail off, and go, ‘So, yeah …’” she said. Brain fog stopped Kristen Tjaden from driving, because she’d forget her destination en route. For more than a year, she couldn’t read, either, because making sense of a series of words had become too difficult. Angela Meriquez Vázquez told me it once took her two hours to schedule a meeting over email: She’d check her calendar, but the information would slip in the second it took to bring up her inbox. At her worst, she couldn’t unload a dishwasher, because identifying an object, remembering where it should go, and putting it there was too complicated.

Memory suffers, too, but in a different way from degenerative conditions like Alzheimer’s. The memories are there, but with executive function malfunctioning, the brain neither chooses the important things to store nor retrieves that information efficiently. Davis, who is part of the Patient-Led Research Collaborative, can remember facts from scientific papers, but not events. When she thinks of her loved ones, or her old life, they feel distant. “Moments that affected me don’t feel like they’re part of me anymore,” she said. “It feels like I am a void and I’m living in a void.”

Most people with brain fog are not so severely affected, and gradually improve with time. But even when people recover enough to work, they can struggle with minds that are less nimble than before. “We’re used to driving a sports car, and now we are left with a jalopy,” Vázquez said. In some professions, a jalopy won’t cut it. “I’ve had surgeons who can’t go back to surgery, because they need their executive function,” Monica Verduzco-Gutierrez, a rehabilitation specialist at UT Health San Antonio, told me.

Robertson, meanwhile, was studying theoretical physics in college when she first got sick, and her fog occluded a career path that was once brightly lit. “I used to sparkle, like I could pull these things together and start to see how the universe works,” she told me. “I’ve never been able to access that sensation again, and I miss it, every day, like an ache.” That loss of identity was as disruptive as the physical aspects of the disease, which “I always thought I could deal with … if I could just think properly,” Robertson said. “This is the thing that’s destabilized me most.”

Robertson predicted that the pandemic would trigger a wave of cognitive impairment in March 2020. Her brain fog began two decades earlier, likely with a different viral illness, but she developed the same executive-function impairments that long-haulers experience, which then worsened when she got COVID last year. That specific constellation of problems also befalls many people living with HIV, epileptics after seizures, cancer patients experiencing so-called chemo brain, and people with several complex chronic illnesses such as fibromyalgia. It’s part of the diagnostic criteria for myalgic encephalomyelitis, also known as chronic fatigue syndrome, or ME/CFS—a condition that Davis and many other long-haulers now have. Brain fog existed well before COVID, affecting many people whose conditions were stigmatized, dismissed, or neglected. “For all of those years, people just treated it like it’s not worth researching,” Robertson told me. “So many of us were told, Oh, it’s just a bit of a depression.

Several clinicians I spoke with argued that the term brain fog makes the condition sound like a temporary inconvenience and deprives patients of the legitimacy that more medicalized language like cognitive impairment would bestow. But Aparna Nair, a historian of disability at the University of Oklahoma, noted that disability communities have used the term for decades, and there are many other reasons behind brain fog’s dismissal beyond terminology. (A surfeit of syllables didn’t stop fibromyalgia and myalgic encephalomyelitis from being trivialized.)

For example, Hellmuth noted that in her field of cognitive neurology, “virtually all the infrastructure and teaching” centers on degenerative diseases like Alzheimer’s, in which rogue proteins afflict elderly brains. Few researchers know that viruses can cause cognitive disorders in younger people, so few study their effects. “As a result, no one learns about it in medical school,” Hellmuth said. And because “there’s not a lot of humility in medicine, people end up blaming patients instead of looking for answers,” she said.

People with brain fog also excel at hiding it: None of the long-haulers I’ve interviewed sounded cognitively impaired. But at times when her speech is obviously sluggish, “nobody except my husband and mother see me,” Robertson said. The stigma that long-haulers experience also motivates them to present as normal in social situations or doctor appointments, which compounds the mistaken sense that they’re less impaired than they claim—and can be debilitatingly draining. “They’ll do what is asked of them when you’re testing them, and your results will say they were normal,” David Putrino, who leads a long-COVID rehabilitation clinic at Mount Sinai, told me. “It’s only if you check in on them two days later that you’ll see you’ve wrecked them for a week.”

“We also don’t have the right tools for measuring brain fog,” Putrino said. Doctors often use the Montreal Cognitive Assessment, which was designed to uncover extreme mental problems in elderly people with dementia, and “isn’t validated for anyone under age 55,” Hellmuth told me. Even a person with severe brain fog can ace it. More sophisticated tests exist, but they still compare people with the population average rather than their previous baseline. “A high-functioning person with a decline in their abilities who falls within the normal range is told they don’t have a problem,” Hellmuth said.

This pattern exists for many long-COVID symptoms: Doctors order inappropriate or overly simplistic tests, whose negative results are used to discredit patients’ genuine symptoms. It doesn’t help that brain fog (and long COVID more generally) disproportionately affects women, who have a long history of being labeled as emotional or hysterical by the medical establishment. But every patient with brain fog “tells me the exact same story of executive-function symptoms,” Hellmuth said. “If people were making this up, the clinical narrative wouldn’t be the same.”

Earlier this year, a team of British researchers rendered the invisible nature of brain fog in the stark black-and-white imagery of MRI scans. Gwenaëlle Douaud at the University of Oxford and her colleagues analyzed data from the UK Biobank study, which had regularly scanned the brains of hundreds of volunteers for years prior to the pandemic. When some of those volunteers caught COVID, the team could compare their after scans to the before ones. They found that even mild infections can slightly shrink the brain and reduce the thickness of its neuron-rich gray matter. At their worst, these changes were comparable to a decade of aging. They were especially pronounced in areas such as the parahippocampal gyrus, which is important for encoding and retrieving memories, and the orbitofrontal cortex, which is important for executive function. They were still apparent in people who hadn’t been hospitalized. And they were accompanied by cognitive problems.

Although SARS-CoV-2, the coronavirus that causes COVID, can enter and infect the central nervous system, it doesn’t do so efficiently, persistently, or frequently, Michelle Monje, a neuro-oncologist at Stanford, told me. Instead, she thinks that in most cases the virus harms the brain without directly infecting it. She and her colleagues recently showed that when mice experience mild bouts of COVID, inflammatory chemicals can travel from the lungs to the brain, where they disrupt cells called microglia. Normally, microglia act as groundskeepers, supporting neurons by pruning unnecessary connections and cleaning unwanted debris. When inflamed, their efforts become overenthusiastic and destructive. In their presence, the hippocampus—a region crucial for memory—produces fewer fresh neurons, while many existing neurons lose their insulating coats, so electric signals now course along these cells more slowly. These are the same changes that Monje sees in cancer patients with “chemo fog.” And although she and her team did their COVID experiments in mice, they found high levels of the same inflammatory chemicals in long-haulers with brain fog.

Monje suspects that neuro-inflammation is “probably the most common way” that COVID results in brain fog, but that there are likely many such routes. COVID could possibly trigger autoimmune problems in which the immune system mistakenly attacks the nervous system, or reactivate dormant viruses such as Epstein-Barr virus, which has been linked to conditions including ME/CFS and multiple sclerosis. By damaging blood vessels and filling them with small clots, COVID also throttles the brain’s blood supply, depriving this most energetically demanding of organs of oxygen and fuel. This oxygen shortfall isn’t stark enough to kill neurons or send people to an ICU, but “the brain isn’t getting what it needs to fire on all cylinders,” Putrino told me. (The severe oxygen deprivation that forces some people with COVID into critical care causes different cognitive problems than what most long-haulers experience.)

None of these explanations is set in stone, but they can collectively make sense of brain fog’s features. A lack of oxygen would affect sophisticated and energy-dependent cognitive tasks first, which explains why executive function and language “are the first ones to go,” Putrino said. Without insulating coats, neurons work more slowly, which explains why many long-haulers feel that their processing speed is shot: “You’re losing the thing that facilitates fast neural connection between brain regions,” Monje said. These problems can be exacerbated or mitigated by factors such as sleep and rest, which explains why many people with brain fog have good days and bad days. And although other respiratory viruses can wreak inflammatory havoc on the brain, SARS-CoV-2 does so more potently than, say, influenza, which explains both why people such as Robertson developed brain fog long before the current pandemic and why the symptom is especially prominent among COVID long-haulers.

Perhaps the most important implication of this emerging science is that brain fog is “potentially reversible,” Monje said. If the symptom was the work of a persistent brain infection, or the mass death of neurons following severe oxygen starvation, it would be hard to undo. But neuroinflammation isn’t destiny. Cancer researchers, for example, have developed drugs that can calm berserk microglia in mice and restore their cognitive abilities; some are being tested in early clinical trials. “I’m hopeful that we’ll find the same to be true in COVID,” she said.

Biomedical advances might take years to arrive, but long-haulers need help with brain fog now. Absent cures, most approaches to treatment are about helping people manage their symptoms. Sounder sleep, healthy eating, and other generic lifestyle changes can make the condition more tolerable. Breathing and relaxation techniques can help people through bad flare-ups; speech therapy can help those with problems finding words. Some over-the-counter medications such as antihistamines can ease inflammatory symptoms, while stimulants can boost lagging concentration.

“Some people spontaneously recover back to baseline,” Hellmuth told me, “but two and a half years on, a lot of patients I see are no better.” And between these extremes lies perhaps the largest group of long-haulers—those whose brain fog has improved but not vanished, and who can “maintain a relatively normal life, but only after making serious accommodations,” Putrino said. Long recovery periods and a slew of lifehacks make regular living possible, but more slowly and at higher cost.

Kristen Tjaden can read again, albeit for short bursts followed by long rests, but hasn’t returned to work. Angela Meriquez Vázquez can work but can’t multitask or process meetings in real time. Julia Moore Vogel, who helps lead a large biomedical research program, can muster enough executive function for her job, but “almost everything else in my life I’ve cut out to make room for that,” she told me. “I only leave the house or socialize once a week.” And she rarely talks about these problems openly because “in my field, your brain is your currency,” she said. “I know my value in many people’s eyes will be diminished by knowing that I have these cognitive challenges.”

Patients struggle to make peace with how much they’ve changed and the stigma associated with it, regardless of where they end up. Their desperation to return to normal can be dangerous, especially when combined with cultural norms around pressing on through challenges and post-exertional malaise—severe crashes in which all symptoms worsen after even minor physical or mental exertion. Many long-haulers try to push themselves back to work and instead “push themselves into a crash,” Robertson told me. When she tried to force her way to normalcy, she became mostly housebound for a year, needing full-time care. Even now, if she tries to concentrate in the middle of a bad day, “I end up with a physical reaction of exhaustion and pain, like I’ve run a marathon,” she said.

Post-exertional malaise is so common among long-haulers that “exercise as a treatment is inappropriate for people with long COVID,” Putrino said. Even brain-training games—which have questionable value but are often mentioned as potential treatments for brain fog—must be very carefully rationed because mental exertion is physical exertion. People with ME/CFS learned this lesson the hard way, and fought hard to get exercise therapy, once commonly prescribed for the condition, to be removed from official guidance in the U.S. and U.K. They’ve also learned the value of pacing—carefully sensing and managing their energy levels to avoid crashes.

Vogel does this with a wearable that tracks her heart rate, sleep, activity, and stress as a proxy for her energy levels; if they feel low, she forces herself to rest—cognitively as well as physically. Checking social media or responding to emails do not count. In those moments, “you have to accept that you have this medical crisis and the best thing you can do is literally nothing,” she said. When stuck in a fog, sometimes the only option is to stand still.

Is the COVID-19 pandemic over?

President Joe Biden said that the pandemic has ended. Here’s what scientists say.

(Update 9/22/2022)

After more than two and a half years of COVID-19 restrictions and mandates, many people are yearning for an official nod that marks the pandemic’s end. And watching the news last week could have led many to conclude that we’ve finally reached that point.

World Health Organization Director-General Tedros Adhanom Ghebreyesus told reporters at a press conference that the end of the pandemic is in sight. A few days later, United States President Joe Biden declared during an interview on 60 Minutes, “The pandemic is over.” But he also acknowledged, “We still have a problem with COVID. We’re still doing a lot of work on it.”

A pandemic is a disease outbreak spanning several countries that affects many people. The WHO is responsible for declaring when an outbreak has grown into a pandemic and deciding when it stops being a public health emergency of international concern. Worldwide, COVID-19 is still causing nearly 1,600 deaths each day and case numbers haven’t plateaued at a low level, leading WHO’s chief scientist, Soumya Swaminathan, to conclude, “It’s still a little premature to say that we’re over it.”

A volunteer in full PPE disinfects an empty street in Chengdu, Sichuan Province, China.
A volunteer disinfects a street in Chengdu, Sichuan Province, China, on September 3, 2022. The city of Chengdu is under lockdown because of the virus.PHOTOGRAPH BY CFOTO, FUTURE PUBLISHING/GETTY IMAGES

In the U.S. the virus is killing between 400 and 500 people daily. “That’s still too many,” says epidemiologist Jennifer Nuzzo, who is the director of Brown University’s Pandemic Center. Others agree with Nuzzo, adding that declaring the end of the pandemic may compromise ongoing testing and vaccination efforts as the highly contagious Omicron BA.5 continues to circulate in the U.S. and many parts of the world, and as cases may rise as more people gather indoors in cooler weather.

Complicating matters, say some epidemiologists, is that there aren’t established criteria—an acceptable level of cases and deaths, for example—to use to determine whether the pandemic is over. While it’s true that humans are more resistant to SARS-CoV-2—through vaccination and or COVID-19 infection—says Eric Topol, founder and director of Scripps Research Translational Institute in California, “the virus is still ahead of us.” To him, the end of the pandemic isn’t imminent, and “that’s for sure.”

What factors tell us when the pandemic is over

While the number of daily deaths is one metric to gauge whether the pandemic is coming to an end, others include case numbers, seasonality of outbreaks, vaccination rates, availability of effective treatments, and the transmissibility of current and new COVID-19 variants. But drawing such conclusions will be complicated, Swaminathan says. “This is a new virus, and we haven’t had a global coronavirus pandemic before.”

Another confounding element is the lack of data from many countries, she says. Figuring out when the pandemic shifts from its acute phase to an endemic one, meaning that COVID-19 is still around but not causing large outbreaks, might only be able to be determined retrospectively. “We may be able to look back and say it was the summer of 2023, for example, that the world came out of the effects of the pandemic.”

A primary school student receives a COVID-19 vaccination in Bangladesh.
A child from Kanishail Primany School in Sylhet, Bangladesh, receives a COVID-19 shot during vaccination program on August 28, 2022.PHOTOGRAPH BY MD RAFAYAT HAQUE KHAN, EYEPIX GROUP/FUTURE PUBLISHING/GETTY IMAGES

For Topol, that judgment has to be based on the trajectory of the pandemic. “I look at where we were in summer 2021—we were down to 12,000 [daily] cases in the U.S. and deaths were just over 200,” he says. “If we held there,” Topol says, he’d be comfortable declaring the pandemic phase over. “But we’re nowhere near that.” Topol also fears that new variants may cause another wave of cases and hospitalizations enabling the pandemic to drag on.

To Lone Simonsen, an epidemiologist at Roskilde University in Denmark, the seasonality of outbreaks, in addition to fewer deaths, could help indicate when the pandemic might end. If case numbers soar in the summer, when the virus has fewer opportunities to spread, “we’re still in the pandemic phase,” she says. That was the case in 2021, when cases were driven by the Delta variant and this past summer with Omicron. So, for Simonsen, it’s a wait and see.

But Denmark and other European countries with high levels of vaccination scrapped most pandemic mandates and restrictions months ago, as COVID-19 hasn’t been causing severe illness or overwhelming hospitals. However, long COVID remains a concern, Simonsen says.

Amesh Adalja, an infectious disease specialist at the Johns Hopkins Center for Health Security argues that the global pandemic phase is largely over given that hundreds of millions of people have already been infected by the virus, there are vaccines and treatments that can prevent severe illness, and COVID-19 is unlikely to completely disrupt the healthcare system like it once did. “It doesn’t mean all of a sudden things go back to 2019. It doesn’t mean that COVID-19 disappears, and all action stops,” he says. “It means there is going to be a baseline number of cases, hospitalizations, and deaths.”

What those acceptable levels of hospitalizations and deaths may be is a political decision, says David Heymann, an infectiousdisease epidemiologist at the London School of Hygiene and Tropical Medicine and former head of WHO’s communicable diseases cluster.

Saying it is over when it isn’t

Nuzzo and others worry that statements like the pandemic is over may be a disservice.

With the U.S. rolling out an Omicron specific booster, “I’m really worried this is going to send out a signal to millions of Americans who are at the risk of severe illness that they may not need to get boosted,” Nuzzo says. “That’s really, really unfortunate.” (See 6 big questions about the new Omicron-targeting booster answered.)

She is also concerned that such statements may lead to a greater reduction in access to free COVID-19 testing and treatments, especially for those uninsured.

Topol worries that it could also undermine the motivation and funding to ramp up development of better COVID-19 vaccines and treatments, jeopardizing the health of millions who are immunocompromised or at the risk of developing long COVID.

This isn’t the right time to make bold assertions about the end of the pandemic, he says. “But it’s time to be bold about accelerating to a point where we look to say, we nailed it, we did it.”

Could COVID-19 trigger depression?

Experts say yes—but not for the reasons you might expect.

(Update 10/16/2022 )

When Glo Lindenmuth was sick with COVID-19 in December 2021, she was congested and exhausted for about a week; her sense of smell and taste were gone for two weeks. She knew about these symptoms before she caught the virus and wasn’t surprised by them. But the sadness and trouble sleeping that kicked in weeks after she recovered from COVID caught her off-guard.

“I had depression as a teenager, but this was much worse,” says Lindenmuth, 30, who works in corporate communications in New York City. In addition to suddenly feeling down, she had trouble sleeping and bad dreams. When she was awake, her brain was foggy and bleak thoughts—often about doing something harmful to herself—intruded. And though she was typically bubbly and extroverted, she was overwhelmed with social anxiety. “I’d cancel plans with friends, sleep all day on the weekends, and avoid the majority of calls and texts,” she says.

Her symptoms lasted for more than two months.

In the spring, Lindenmuth began feeling a bit better but then another intense wave of depression enveloped her from mid-June to mid-August. That’s when she went to see a behavioral psychiatrist who diagnosed her with depression.

It’s estimated that millions of people are discovering that even after they think they have bounced back from their COVID-19 illness, they continue to feel down, fatigued, apathetic, anxious, or otherwise emotionally out of sorts.

In a study based on millions of people who used the U.S. Department of Veterans Affairs health system, “we noticed that we had a nation in distress, due to the mayhem of the pandemic and lockdown,” says Ziyad Al-Aly, director of the clinical epidemiology center at Washington University in St. Louis, Missouri, and a coauthor of the report. Al-Aly and his colleagues wanted to know whether people who got COVID-19 had a higher risk of mental health problems after symptoms of the illness subsided. “The answer was absolutely yes. People with COVID had it much, much worse.” 

According to research in the June 2022 issue of the journal CNS Drugs, 35 percent of people reported depressive symptoms after recovering from COVIDAnd it may not be simply because they lost days or weeks of their regularly scheduled lives to COVID. It may be because they have a little-known phenomenon called post-viral depression, which is likely triggered by inflammatory changes, psychological stress, and other factors.

These symptoms typically “kick in two to three months after the onset of COVID-19 and seem to last several months,” says Madhukar Trivedi, a psychiatrist and founding director of the Center for Depression Research and Clinical Care at the UT Southwestern Medical Center in Dallas. “There’s no way to predict who will have transient effects or who will have persistent ones.” 

The scope of the phenomenon

The link between viral illnesses and depression isn’t new but has become more widely recognized and understood in recent decades. A study in a 2016 issue of the journal Brain, Behavior, and Immunity, for example, found that people who were sick with the flu in the previous 30 to 180 days had a 57 percent higher risk of new onset depression, compared to those who dodged the virus. Post-viral depression also can happen with the Epstein-Barr virus, which causes mononucleosis, and other non-specific viruses, experts say.

Al-Aly’s study, published in February 2022 in BMJfound that people who’d been sick with COVID had a 35 percent higher risk of developing an anxiety disorder and a 39 percent higher risk of experiencing a bout of depression a month after their illness; these surges were accompanied by increased use of antidepressants and benzodiazepines.

This is far from an isolated finding. A study in the April 2022 issue of the Journal of Neurology found that elevated levels of apathy and anxiety were common among COVID survivors who had fatigue eight months after their illness. And in a study in the May 2022 issue of The Lancetresearchers followed the mental-health trajectory of people in six countries in Europe who had been sick with COVID—but weren’t hospitalized for it—and found that these individuals had a higher prevalence of depression in the subsequent months, especially if they had been bedridden with the illness.

Mechanisms behind the misery

Exactly how COVID-19 triggers depression isn’t fully understood but there are several hypotheses. The SARS-CoV-2 virus may cause more inflammation in the brain and activate microglial cells, immune cells in the central nervous system that produce inflammatory molecules, Al-Aly explains. “Inflammation can affect brain regions that regulate affect and emotions—it can turn them up or turn them down.” 

Another theory is that the virus can attack the lining of blood vessels, which can compromise the blood and oxygen supply to the brain and disrupt areas that regulate emotion, Al-Aly adds. 

A third hypothesis suggests that the virus can disrupt the diversity and equilibrium of the bacteria in the gut—the gut microbiome—which could in turn alter the levels of certain neurotransmitters, chemical messengers that transmit nerve signals throughout the body and brain and are involved in mood regulation, he says. “What’s really clear is that the virus’s effect on mental health is a biological phenomenon—it’s not imagined,” Al-Aly says. 

That’s not to say there aren’t psychological elements at play. Prolonged isolation and feelings of loneliness during the illness may contribute to post-COVID depression, says Pravesh Sharma, a psychiatrist at the Mayo Clinic College of Medicine and Sciences in Eau Claire, Wisconsin. When it comes to post-COVID depression, “sometimes people think why me?” Sharma says. “That creates a lot of negative thought and affects how people function in everyday life.” These factors can trigger a vicious cycle that traps people in a depressive state.

Compounding the problem, people with post-COVID depression often feel misunderstood. “Their families don’t understand why they’re not over it because they’re not sick anymore,” says Dawn Potter, a clinical psychologist who runs support groups for people with long COVID at the Cleveland Clinic. Plus, these “people don’t know when their symptoms are going to end or what’s going to help, and they’re scared. And it’s common for people to be afraid of getting COVID again.” Some people also worry about the potential long-term effects of COVID infection, which can contribute to their emotional turmoil after being sick, experts say. 

Who’s vulnerable and why

While research on the issue is scarce because COVID-19 is still relatively new, experts believe that people who have a prior history of depression or anxiety are at higher risk of developing post-COVID depression. “What I’m seeing in my clinical practice is people getting depression after COVID or having it be exacerbated by COVID if they had depression before,” says Potter. “It may have been in remission or less severe.”

Others who are at higher risk for post-COVID depression, experts say, include people who had high levels of pre-infection stress, medical morbidities—obesity, asthma, hypertension, diabetes, and the like—and more severe illness with COVID-19. 

In some instances, depression can occur as part of long COVID syndrome, which can include lingering problems with memory, thinking abilities and concentration, mood changes, fatigue, and organizational abilities such as difficulty managing medication or money. Dyani Lewis, 44, experienced this phenomenon firsthand after getting COVID in March of 2022. Despite having a mild case—“I’ve had colds worse than this,” she says—about a week after the infection passed, she had daily headaches, dizziness that felt like perpetual motion sickness, fatigue, and a lack of motivation. She had been taking a selective serotonin reuptake inhibitor (SSRI) for depression since 2019 and her mood symptoms had been well-controlled—until suddenly they weren’t.

“I was struggling to complete my work, and I didn’t have energy for my kids,” says Lewis, a freelance science journalist and mother of two daughters in Melbourne, Australia. “To what extent SARS-CoV-2 directly exacerbated my depression, or just created the circumstances that were ripe for me to feel like shit, I don’t know.” Lewis is in the process of switching to a new medication for her depression and has started resuming light exercise, to improve her mood and boost her energy.

Experts say they’re not seeing clear gender patterns with post-COVID depression. But a study in the January 2022 issue of the Journal of Psychiatric Researchfound that among COVID-19 survivors in Italy who experienced psychiatric symptoms, men had high levels of anxiety and depression at six months and even more severe symptoms at 12 months; women experienced the worst depression shortly after the infection, but by six months the symptoms were much less serious and continued to decline until 12 months. The researchers noted that this may be because men have a stronger pro-inflammatory immune response than women do, which could lead to sustained inflammation in their brains and bodies after COVID infection. Another explanation is that they’re less likely to seek professional help for mental health challenges.

Reclaiming a better state of mind

Although some cases of post-COVID depression will resolve naturally over time, there’s no reason to sit back and suffer in the meantime. “It’s important not to say this is due to COVID and therefore do nothing,” Trivedi says, “because it could last longer than you think.”

To feel better mentally and emotionally, it helps to engage in regular physical activity or exercise, which has anti-inflammatory properties as well as antidepressant effects, Trivedi says. Seek social support, by connecting with friends and family members and/or support groups in your community. And adopt healthy eating habits such as the Mediterranean diet—which is rich in fruits, vegetables, legumes, nuts, whole grains, fish, and olive oil—because research has found that it’s associated with a lower risk of developing depression. In addition, a study in a 2019 issue of the journal PLoS One found that a healthy dietary intervention can start to work in as little as three weeks, reducing symptoms of depression.

It’s also important to set the stage for better sleep because “sleep problems and depression go hand in hand—it’s a bidirectional issue,” Potter says. Simply put, poor sleep can affect your mood, and depression can compromise your sleep quality. “If you can start sleeping better, it often helps mood,” she says. To that end, she recommends working on your pre-sleep habits, making a concerted effort to dim the lights, avoid digital screens in the evening, and go to bed and wake up at the same time, day after day, to maintain a consistent sleep-wake cycle.

There’s no need to stop your feel-better efforts with lifestyle modifications. Depending on the severity of your symptoms, you may benefit from therapy, particularly cognitive behavioral therapy (CBT)—which helps people shift detrimental thought patterns to more helpful ones. Another helpful approach is behavioral activation, a skill that’s often incorporated into CBT and involves setting goals that will help you get out and do things that can improve your mood, says Jed Magen, an osteopathic physician specializing in child and adolescent psychiatry at Michigan State University in East Lansing.

With the help of antidepressants, talk therapy, and sharing her experiences with her social network, Lindenmuth started to feel better. Gradually she began exercising more and rediscovered her love of cooking, dancing, and spending time with friends. “Now I’m feeling great, and I have the energy I used to,” she says. “I’ve also regained my creativity as well as a sense of clarity that I haven’t had in a long time,” Lindenmuth says. “I’m happy to be on the other side of the worst of it.”

When it comes to experiencing post-COVID depression and obtaining relief from it, Lindenmuth is in good company. “I would like people to know that post-COVID depression is very, very common and that there’s hope—the research is showing that there are ways to treat post-COVID depression, just like there are for other forms of depression,” Potter says. “Even though it’s not completely understood, we’re not reinventing the wheel.”

‘Speed of Science’ — A Scandal Beyond Your Wildest Nightmare

It was never about science or protecting others.

(Update 10/27/2022)

Small admitted that Pfizer never tested whether their jab would prevent transmission because they had to “move at the speed of science to understand what is happening in the market … and we had to do everything at risk” (Billion Photos/Shutterstock)

It was never about data or science; it was about following the top-down script they had from the beginning. And this recent admission by a Pfizer executive proves it would be called out as fraudulent in any other industry. So how have they managed to pull the wool over so many people’s eyes?


  • The premise behind COVID shot mandates and vaccine passports was that by taking the shot, you would protect others, as it would prevent infection and spread of COVID-19
  • In early October 2022, during a COVID hearing in the European Parliament, Dutch member Rob Roos questioned Pfizer’s president of international developed markets, Janine Small, about whether Pfizer had in fact tested and confirmed that their mRNA jab would prevent transmission prior to its rollout
  • Small admitted that Pfizer never tested whether their jab would prevent transmission because they had to “move at the speed of science to understand what is happening in the market … and we had to do everything at risk”
  • We’ve known for well over two years that the shots were never tested for transmission interruption. In October 2020, Peter Doshi, associate editor of The BMJ, highlighted that trials were not designed to reveal whether the vaccines would prevent transmission. Yet everyone in government and media insisted they would do just that
  • It was never about science or protecting others. It was always about following a predetermined narrative that sought to get experimental mRNA technology into as many people as possible

February 9, 2021, I published an article that clarified the medical and legal definitions of a “vaccine.” In the article, I noted that mRNA COVID-19 jabs did not meet those definitions, in part because they don’t prevent infection or spread. In reality, they’re experimental gene therapies. In July that year, The New York Times published a hit piece on me citing that February 9 article:1

“The article that appeared online on Feb. 9 began with a seemingly innocuous question about the legal definition of vaccines. Then over its next 3,400 words, it declared coronavirus vaccines were ‘a medical fraud’ and said the injections did not prevent infections, provide immunity or stop transmission of the disease.

Instead, the article claimed, the shots ‘alter your genetic coding, turning you into a viral protein factory that has no off-switch.’ Its assertions were easily disprovable …”

Pfizer Moved ‘at the Speed of Science’

Fast-forward to early October 2022, and my claims were officially confirmed during a COVID hearing in the European Parliament. Dutch member Rob Roos questioned Pfizer’s president of international developed markets, Janine Small, about whether Pfizer had in fact tested and confirmed that their mRNA jab would prevent transmission prior to its rollout.

As noted by Roos, the entire premise behind COVID shot mandates and vaccine passports was that by taking the shot, you would protect others, as it would prevent infection and spread of COVID-19. Small replied:

“No. We had to really move at the speed of science to understand what is happening in the market … and we had to do everything at risk.”2

This means the COVID passport was based on a big lie. The only purpose of the COVID passport: forcing people to get vaccinated. I find this shocking — even criminal. 

— Rob Roos, MEP

As noted by Roos, “This means the COVID passport was based on a big lie. The only purpose of the COVID passport: forcing people to get vaccinated.” Roos added that he found this deception “shocking — even criminal.”3

In the video below, biologist and nurse teacher John Campbell, Ph.D., reviews this growing scandal. He points out that U.K. government officials emphatically assured the public that everything that was normally done in clinical trials for a vaccine was done for the COVID shots. Now we’re told that was not the case after all.

The question is why? According to Small, these basic trials were not done because they “had to move at the speed of science.” But just what does that mean? As noted by Campbell, these are “just words without meaning.” It’s complete nonsense.

Moreover, what does it mean to “do everything at risk”? Campbell admits he has no idea what that means. I don’t either, but were I to venture a guess, I’d guess it means they knowingly skipped certain testing even though they knew the risks of doing so.

Government and Media Promulgated a Blatant Lie

Over the past three years, mainstream media have promulgated the lie that the COVID shots will prevent infection and transmission, telling us that anyone who doesn’t get the shot is selfish at best, and at worst, a potential murderer at large. Anyone who refuses poses a serious biomedical threat to society, hence the need for heavy-handedness.

Alas, it was all a lie from the start. The frustrating part is that we’ve KNOWN for well over two years that the shots were never tested for transmission interruption, yet everyone in government and media insisted they would do just that.

In October 2020, Peter Doshi, associate editor of The BMJ, highlighted the fact that the trials were not designed to reveal whether the vaccines would prevent transmission, which is key if you want to end the pandemic. He wrote:4

“None of the trials currently under way are designed to detect a reduction in any serious outcome such as hospital admissions, use of intensive care, or deaths. Nor are the vaccines being studied to determine whether they can interrupt transmission of the virus.”

So, by October 2020, at the latest, it was clear that no studies had been done to determine whether the shots actually prevented transmission, which is a prerequisite for the claim that you’ll save the lives of others if you take it.

By then, Moderna had also admitted they were not testing its jab’s ability to prevent infection. Tal Zaks, chief medical officer at Moderna, stated that this kind of trial would require testing volunteers twice a week for long periods of time — a strategy he called “operationally untenable.”5

So, neither Pfizer nor Moderna had any clue whether their COVID shots would prevent transmission or spread, as that was never tested, yet with the aid of government officials and media, they led the public to believe they would. Below is just one example where Pfizer clearly obfuscated the truth.6 If stopping transmission was their “highest priority,” why didn’t they test and confirm that their shot was accomplishing this priority?

Similarly, in an Israeli interview7 (below), Bourla stated that “The efficacy of our vaccine in children is 80%.” The reporter asked him to clarify, “Are you talking about efficacy to prevent severe disease or to prevent infection?” and Bourla replied, “To prevent infection.” How could he say that when preventing infection has never been tested? Is that not evidence of fraud, caught on camera?

As I stated in February 2021, the shots are a medical fraud. A true vaccine prevents infection; COVID shots don’t. Hence, they’ve also been fraudulently marketed. Governments around the world enabled this marketing fraud and media promulgated it.

As a result of mandating COVID shots and vaccine passports based on a blatant lie, millions have suffered potentially permanent harm and/or have died. Millions have also lost their jobs, forfeited careers and missed out on educational opportunities. This all happened because we DIDN’T follow the science.

Massive Conflicts of Interest Have Been Allowed

Why did government agencies go along with what was, to anyone with a microgram of critical thinking skills, an apparent fraud? Probably, because they’re in on it. As reported by investigative journalist Paul Thacker, the same PR company that serves Moderna and Pfizer also staffs the U.S. Centers for Disease Control and Prevention’s Division of Viral Diseases team:8

“Early last month [September 2022], CDC Director Rochelle P. Walensky endorsed recommendations by the CDC Advisory Committee on Immunization Practices (ACIP) for updated COVID-19 boosters from Pfizer-BioNTech and Moderna.

‘This recommendation followed a comprehensive scientific evaluation and robust scientific discussion,’ Dr. Walensky said in a statement. ‘If you are eligible, there is no bad time to get your COVID-19 booster and I strongly encourage you to receive it’ …

[The] PR firm Weber Shandwick, which has long represented Pfizer and other pharmaceutical companies and began providing public relations support to Moderna sometime in 2020.

In an odd case of synchronicity — and let’s be honest, a whiff of undue influence — Weber Shandwick employees are also embedded at the CDC’s National Center for Immunization and Respiratory Diseases (NCIRD), the CDC group that implements vaccine programs and oversees the work of ACIP [CDC’s Advisory Committee on Immunization Practices] …

The CDC has refused to respond to questions explaining this apparent conflict … ‘[It] is irresponsible of CDC to issue a PR contract to Weber Shandwick, knowing that the firm also works for Moderna and Pfizer,’ emailed Public Citizen’s Craig Holman. ‘It raises legitimate questions of whose interests Weber Shandwick will put first — their private sector clients or the public’s interest at NCIRD.’”

Incidentally, Weber Shandwick was in 2016 found to have ghostwritten a drug study for Forest Pharmaceuticals — another unethical practice that has undermined the foundation of medical science for decades.

One PR Company, One Consistent Message

Weber Shandwick’s responsibilities at the CDC include but are not limited to “generating story ideas, distributing articles and conducting outreach to news, media and entertainment organizations” to boost vaccination rates.9 The company provides similar services to Moderna.

For example, it helped generate 7,000 news articles internationally after Moderna applied for emergency use authorization (EUA) for its jab.

In June 2022, Moderna announced a “cross-discipline team drawing on talent and expertise from Weber Shandwick” would “drive the brand’s narrative globally,” and “support Moderna in activating and engaging key internal and external audiences, including employees, consumers, health care providers, vaccine recipients and policymakers.”10

Considering the primary COVID jab makers have the same PR company as the CDC, is it any wonder that the messaging has been so consistently one-sided? As noted by Doshi in a recent interview on German television,11 mainstream media have consistently ignored COVID jab data and have “not done a good job in providing balanced coverage” about the shots.

“We’re not getting the information we need to make better choices and to have a more informed understanding of risk and benefit,” he told the interviewer, adding:12

“It was very unfortunate that from the beginning, what was presented to us by public health officials was a picture of great certainty … but the reality was that there were extremely important unknowns.

We entered a situation where essentially the stakes became too high to later present that uncertainty to people. I think that’s what set us off on the wrong foot. Public officials should have been a lot more forthright about the gaps in our knowledge.”

Reanalysis of Trial Data Confirms COVID Shot Dangers

In late September 2022, Doshi published a risk-benefit analysis focused on serious adverse events observed in Pfizer’s and Moderna’s COVID trials. Reanalysis of the data showed 1 in 800 who get a COVID shot suffers a serious injury. As detailed in Doshi’s paper:13

“Pfizer and Moderna mRNA COVID-19 vaccines were associated with an excess risk of serious adverse events of special interest of 10.1 and 15.1 per 10,000 vaccinated over placebo baselines of 17.6 and 42.2 respectively.

Combined, the mRNA vaccines were associated with an excess risk of serious adverse events of special interest of 12.5 per 10,000 vaccinated; risk ratio 1.43.

The Pfizer trial exhibited a 36 % higher risk of serious adverse events in the vaccine group … The Moderna trial exhibited a 6 % higher risk of serious adverse events in the vaccine group … Combined, there was a 16 % higher risk of serious adverse events in mRNA vaccine recipients …”

Doshi and his coauthors also concluded that the increase in adverse events from the shots surpassed the reduction in risk of being hospitalized with COVID-19. So, in short, the shots confer more harm than good.

Sen. Rand Paul Promises Investigation

A spokesperson for Sen. Rand Paul, R-Ky., replied to an inquiry by Thacker stating, “[T]hat CDC had a contract with the same PR firm representing the manufacturers of the COVID-19 vaccine raises serious concerns,” adding that “these conflicts of interest will be thoroughly investigated” by the Senate Committee on Health, Education, Labor and Pensions (HELP) — which oversees the CDC — sometime next year.

After the November midterms, Paul will be next in line as the top Republican on this committee. It’s well worth noting that, at bare minimum, this kind of conflict of interest should have been disclosed by both parties. At best, it should have been avoided altogether. The CDC did neither. It didn’t disclose its relationship with the PR firm and it didn’t prevent the conflict of interest from developing in the first place.

What Was the COVID Jab Push All About?

The rational take-home from all this is that the massive push to inject the global population with these experimental jabs was never about following science and protecting others.

It was always about promoting a false, invented narrative designed to allow for the implementation of a top-down directive to inject every person on the planet with a novel mRNA technology. This, in turn, brings up two central questions:

•Who’s at the top? — We don’t yet know. All we can say for sure is that they have a very powerful and global influence — powerful enough that government officials have willingly lied and sacrificed their own populations in an incredibly risky medical experiment.

•Why is injecting everyone with mRNA technology so important to the anonymous decision-makers? — Again, we don’t know, but it’s quite clear that there’s a reason for it, that it’s supposed to accomplish something.

As detailed in previous articles, the only rational reason for why the CDC is allowing COVID jab EUA’s for young children is because they’re assisting drug makers in their effort to obtain liability shielding by getting the shots onto the childhood vaccination schedule.

ACIP is poised to add COVID shots to the childhood vaccination schedule any day now,14 and once on the childhood schedule, vaccine makers will not be liable for injuries and deaths occurring from their shots, whether they occur in children or adults.

Also, remember that even though the U.S. Food and Drug Administration granted full approval to Pfizer’s Comirnaty COVID shot, Comirnaty was never released to the public. The Pfizer shot being given is still under EUA.

Why was Comirnaty never released? Probably because once the shot has full FDA approval, liability kicks in. It appears they’re trying to avoid liability by getting the EUA shot on the childhood schedule before Comirnaty is rolled out and starts injuring and killing people.

Now, if they’re concerned about liability, that means they know the shot is dangerous. And if they know it’s dangerous (which all available data clearly show it is), then why do they want every person on the planet to get it?

Following this line of questioning to its logical conclusion leads us to the shocking conclusion that even though we don’t know the reasons why, the injuries and deaths from these jabs could be intentional?

Vaccine Makers Continue to Spread Lies

Despite Small’s unequivocally clear admission that Pfizer has not tested its COVID shot to ascertain whether it prevents transmission, Pfizer’s CEO still does not shy away from insinuating as much. Here’s what he tweeted out October 12, 2022.15 He’s not saying the shot has been confirmed to prevent COVID, but he insinuates that it does by saying the FDA authorized it for the prevention of COVID. This is also known as lying by omission.

Meanwhile, so-called fact checkers are trying to salvage Pfizer’s reputation by saying the company never actually stated the shot would stop transmission.16 That may be so, but government officials and media DID claim it would prevent both infection and spread, and Pfizer never corrected them, even as people were being fired and ostracized from society for not taking the jab.

If they were truly on the up-and-up, Pfizer officials would have clarified that the shot had not been tested to confirm it would prevent transmission, and until that was known, mandates and passports had no basis. Pfizer didn’t do that. Instead, they went along with it.

In conclusion, there’s no reason to trust government ever again, at least not in the U.S., which stands alone in pushing the jab on toddlers. (The reason for that, as mentioned earlier, is probably to get the jabs onto the childhood vaccination schedule, which will shield the vaccine makers from financial liability for harms.)

As noted by GB News host Neil Oliver in the video above, the very basis for COVID mandates or vaccine passports — that everyone had to get jabbed for the greater good, to protect others and help end the pandemic — was a deliberate lie from the start.

Many of us realized this early on, but our voices were drowned out as government, Big Tech and media pulled out all the stops, censoring anyone who told the truth. And all who have participated in this grand deception remain unrepentant to this day.

In a recent Twitter thread, a Twitter user named Daniel Hadas lays out an excellent description of what the last three years were really about:17

“The debate over whether, when, and to what extent lies were told about COVID vaccines preventing transmission misses a central point: No matter what the trial data showed, the vaccines were ALWAYS going to be pushed on entire populations, by fair means or foul.

Very early on, the COVID response was locked into a specific narrative. The world would lock down and stay safe, while brave scientists hammered away at a vaccine … You may recall that, in the first months of COVID, there was a lot of breathless talk about whether there would EVER be a vaccine.

This was all nonsense … Our authorities would not have adopted the strategy of lockdown-till-vaccine unless they were certain a vaccine could and would be made …

The purpose of sowing fear that there might never be a vaccine was to increase gratitude and enthusiasm when one came along. Indeed, every part of the early COVID response can be understood as (in part) pre-release marketing for the vaccine …

That’s why COVID risks for the young were wildly amplified. That’s why there was unending obfuscation of the central role of infection-conferred immunity both in protecting individuals and in ending the pandemic.

The plan was that the vaccine would be met by a perfectly primed population: immunologically naive, desperate to be released from lockdowns, terrified of COVID, eager to do the right thing, i.e. protect others through taking the shots.

Once so much effort had gone into priming, it is UNIMAGINABLE that authorities would have pivoted to telling us … ‘Well, actually, the vaccine’s safety profile is only so-so, efficacy is murky, and most people don’t need to worry about COVID anyway. So best most of you not take this … Sorry about the lockdowns.’

That was not in the script. So it was inevitable that the vaccine be pushed on everyone, and inevitable that the best arguments for universal vaccination would be used. Those arguments were: COVID is super-dangerous for YOU. Distrust in this vaccine is distrust in science. Refusing to get vaccinated is immoral, because you will infect others.

The veracity of these claims didn’t matter: they were in the script, and it was too late to deviate … Accordingly, the stage was also set for vaccine mandates.

None of this is conspiratorial. It is descriptive … Clarifying the details won’t alter the essence of the picture — The COVID response was determined by a script of vaccine salvation, and societies’ investment in that script was too deep for mere realities to divert its execution.”

The primary questions that still remain unanswered are: Why was this script created? What are its intended consequences? And, who created it? As mentioned earlier, the evidence suggests harm is an intended outcome — harm to our economy, our social order, our health, our life span and reproductive capacity.

As for “why,” we can just look at what has been accomplished so far.

Originally published October 24, 2022 on

Sources and References

COVID-19 can interfere with your period in many ways. Here’s how.

Physicians failed to warn women about the expected temporary disruptions to their periods after the vaccine, and the more significant issues after a severe bout of COVID-19.

(Update 10/29/2022)

Raven La Fae, a 31-year-old artist in Calgary, Canada, has always been able to predict her menstrual period almost to the day—arriving every 28 days and lasting for five. But after contracting COVID-19, that’s no longer the case.

La Fae’s bout with the disease felled her for two miserable weeks. Her menstrual cycle landed during that time, so she wasn’t surprised. What stunned her was how long it lasted—10 days.

“My period has been funky ever since,” La Fae laments, and when she contracted COVID again, it became even less predictable. While the days between her cycles have mostly returned to baseline, bleeding lengths have not, lasting up to 13 days a month.

From the beginning of the pandemic, women worldwide began noticing changes to their menstrual cycles. In some cases, this happened after contracting the virus; in others, after receiving a vaccine. With so many women recording their cycles in period-tracking apps, researchers have been able to more easily document the phenomenon.

Physicians were taken off guard. La Fae’s healthcare provider, after determining her hormones were normal, said she couldn’t explain it. Women complained their doctors dismissed their hunch the virus might be linked to disrupted cycles.

“When COVID started we were worried about people dying, so other things were overlooked,” admits Hugh Taylor, chair of obstetrics and gynecology at Yale Medicine. In retrospect, Taylor says, women should have been alerted to this possibility. “We see irregular menstrual cycles with other acute infections, so it isn’t surprising it happens here.”

Poor messaging

Without research or reassurance from physicians, women were alarmed by the deviations in their periods, Taylor says, and for good reason: “We’ve been warning people for years that changes in a period might be a symptom of a hormonal imbalance, or even cancer.”

When girls and women noticed unexpected shifts in their cycle after receiving a COVID shot, some second-guessed their decision to get a vaccine, says Candace Tingen, a program director at the National Institute of Child Health and Human Development, which has awarded $1.67 million to five research institutions to study the issue.

Tingen points out that her institute has long emphasized the importance of menstrual cycles to health. “We talk about it as a fifth vital sign,” she says (the other four being body temperature, blood pressure, pulse, and respiration).

Most concerning to younger women was whether these changes could reduce fertility, Taylor says. It wasn’t until January that a study of 2,000 American couples published in the American Journal of Epidemiology resolved the question. Women trying to conceive who’d had the virus saw no decrease in fertility. Similarly, the COVID shot had no impact on conception rates.

Both virus and vaccine may temporarily alter menstruation

Scientists are still figuring out how many women have seen their menstrual cycles change, but it’s clear the numbers are substantial. In a study of 127 women of childbearing-age in Arizona who had contracted COVID, 16 percent reported some alteration; most common were irregular cycles or longer gaps between bleeds. These shifts were more likely in those whose infection involved more symptoms or was more severe (but not to the point of hospitalization).

In this study, women also had increases in the premenstrual syndrome symptoms of mood changes and fatigue. “We think of the menstrual period as an acute event that occurs for a few days, but hormones are changing throughout the entire cycle,” explains Leslie Farland, an epidemiology professor at the University of Arizona and the study’s principal investigator.

Researchers in other countries report even greater percentages of women suffered changes to their periods after contracting COVID. A United Kingdom survey found nearly half the women reported alterations, primarily in cycle length and increased PMS, as did 47 percent of women from Jordan and Iraq, according to another study from the Middle East.

A study on the vaccine’s effect funded by the National Institutes of Health published in January tracked 4,000 women from the U.S. who used one period tracking app. It found cycles shifted after the first shot, but only by an average of less than a day. Those whose second shot fell in the same cycle shifted by about two days, though in either case the length of bleeding wasn’t altered, says Alison Edelman, an obstetrician and gynecologist at Oregon Health and Science University and the study’s principal investigator. A second study by Edelman, of nearly 20,000 women in North America and Europe using the same app reported similar findings in September.

These slight changes occurred with all brands of the vaccines, and in most cases, they disappeared the following cycle. Still, 10 percent of the women saw their period shift by more than a week after either dose. However, these women were also back to normal soon after.

How does coronavirus change a period?

Exactly how the coronavirus or vaccine affects the menstrual cycle isn’t clear.

One hypothesis posits that COVID-19 may affect what’s known as the hypothalamic-pituitary-ovarian axis. To begin each monthly cycle, the hypothalamus gland signals the pituitary gland to secrete two hormones that together release an egg from the ovaries.

It’s possible the coronavirus affects the hypothalamus directly, Taylor says, but the body may also proactively decrease the activity of these glands if the virus is detected. “This has evolutionary advantages, because you don’t want to get pregnant when you’re fighting off a physical stressor, which could be an illness or malnutrition or the like,” he explains.

Alternatively, the immune system engaged in fighting the virus could alter the normal inflammatory response of the uterine lining (endometrium) during the cycle, researchers recently suggested in the International Journal of Epidemiology.This may be why people who experienced a more intense bout of COVID—indicating a higher viral load and more immune activity—have higher rates of menstrual changes, as the University of Arizona study found.

That was the case for Annette Gillaspie, a 41-year-old registered nurse in Hillsboro, Oregon, who contracted COVID and was extremely ill for more than two weeks. She now has long COVID symptoms, including a fluctuating heart rate and fatigue so extreme a shower can send her to bed for days. Her periods are so unusually long and heavy—gushing for almost two weeks some months—that Gillaspie had a hormonal intrauterine device inserted. So far, it hasn’t reduced her bleeding, and if she doesn’t improve within a few months, she’ll likely have a hysterectomy.

Vaccines trigger more minor shifts

Vaccines trigger the body’s immune system response, albeit a smaller one than the disease, so the same mechanisms could be involved in their temporary menstrual cycle disruptions, Tingen says.

Disseminating this reassuring information to women so they know to expect this possible side effect is an important public health task, Tingen says.

Anyone whose cycle remains significantly altered for several months, however, should check with their healthcare provider, Taylor says. “My suspicion is that people on the cusp of a medical condition—thyroid abnormalities, hormonal irregularities, bleeding from fibroids—might be pushed over the edge” by the coronavirus or COVID vaccine.

Edelman hopes this will be a teaching moment for her profession. “Menstrual health has been woefully understudied, not just in vaccine trials but in almost every area of research,” she says. “Yet half the population will, does, or has menstruated, and this routine biological function has meaning for the individual and for science.”

COVID-19 can ruin your sleep in many different ways—here’s why

Scientists are learning more about the havoc that viruses and bacteria wreak on sleep. Here’s what you need to know about seeking care for insomnia.

(Update 11/10/2022)

Six weeks after a mild case of COVID-19 early in the pandemic, Erika Thornes started waking up every night between 2 and 3 a.m. Unable to fall back asleep, she would listen to podcasts, read, and scroll through Twitter before finally dozing off by 4 or 5 a.m. That was more than two years ago and Thornes, a mother to three teenagers in San Diego, still struggles to sleep through the night every now and then.

A similar thing happened to her husband during a recent COVID infection. He was suddenly waking up at 3 a.m. every night. His sleep improved when he stopped testing positive, but the symptom was extreme while it lasted. “He was quite shocked,” she says. “He knew I was waking up, but I don’t think he quite understood the severity of ‘awake.’”

Nightmares. Days without sleep. Waking in a panic in the middle of the night. Sleeping for 18 hours a day. As COVID-19 has swept through the global population, so too have reports of sleep disruptions both during an infection and in the weeks and months beyond.

The links between COVID and sleep are still under investigation, but studies show that bacterial and viral infections, in general, interfere with sleep through physical and psychological mechanisms. Recognizing the potential for the virus to upset sleep, experts say, can help people get the care they need.

How sleep and the immune system affect each other

Sleep is intricately entwined with the immune system, a link both well-known and still mysterious. Getting enough rest can help prevent infections, according to evidence and observations going back thousands of years. But infections can also disrupt sleep in complicated ways.

Studies in animals show that viruses and bacteria alter both the amount of time spent sleeping and the kind of sleep, says John Axelsson, director of the Sleep Laboratory at Stockholm University’s Stress Research Institute in Sweden. When researchers inject rabbits or rodents with moderate doses of bacteria or viruses, the animals sleep more. They get more non-rapid eye movement sleep, a deep restful state thought to be important for recovery; and they spend less time in dream-filled REM sleep.

Cytokines, a category of molecules that can stimulate or slow down inflammation, appear to play a major role in these patterns, Axelsson says. When healthy animals are sleep deprived, levels of some pro-inflammatory cytokines in the brain rise, causing the animals to sleep more than usual. When scientists block these cytokines, animals don’t sleep more—even when they are sleep deprived.

It’s harder to do the same kind of research in people, and results are mixed about how sleep changes during illnesses. But studies suggest that, at least to some extent, inflammatory molecules affect sleep in ways comparable to other animals. In studies from the 1990s and early 2000s, researcher Thomas Pollmächer and colleagues injected people with bits of bacterial cell walls, called endotoxins, and found that mild activation of the immune system increased the drive for sleep and enhanced non-REM sleep.

But once the immune system revved up with increased cytokine levels and symptoms of illness, people experienced more disrupted sleep, not typically seen in animals. “The inflammatory system increases the drive for sleeping,” Axelsson says. “But at the same time, it then disrupts your sleep if you get a fever.”

To see how respiratory infections affect human sleep, Axelsson and colleagues recruited 100 healthy adults to keep a detailed sleep diary after experiencing the first symptoms of a respiratory infection while wearing a sleep-tracking device on their wrists. Of the 100 volunteers, 28 people got sick. Overall, those people spent longer in bed and slept more after their symptoms began, the researchers reported in 2019.

But this wasn’t a restful sleep. Infected people had difficulty falling asleep, woke up more, and had a more restless sleep especially when they were most symptomatic. As symptoms eased, sleep improved. Anecdotally, that’s the same pattern reported by many people with COVID—a lot of sleep initially followed by insomnia or other disruptions while sickest. The physiological drive to sleep more while getting sick might be adaptive—helping the body fight off the invader, Axelsson says.

Why sleep problems continue after COVID infection

For many people, sleep troubles don’t end on Day 10 or when a person tests negative. To gauge how often sleep troubles persist, researchers surveyed more than 650 long COVID patients who visited the Cleveland Clinic’s reCOVer Clinic between February 2021 and April 2022. Up to six months after an infection, 41 percent reported sleep disturbances; an additional 7 percent reported disturbances that were severe. Black patients, 12 percent of study participants, were three times more likely to report sleep problems compared with other groups—echoing disparities seen throughout the pandemic, says Cinthia Peña Orbea, a sleep specialist and lead author of the study, which was published in June.

Elsewhere, there have been reports of post-COVID narcolepsy, excessive sleeping, and physically enacting dreams with movements like kicking and talking instead of lying still with typical sleep-induced paralysis, says Monika Haack, a psychoneuroimmunologist at Harvard Medical School in Boston, who co-authored a 2019 review of the links between sleep and disease.

Peña Orbea’s study suggests that long COVID falls in line with other chronic illnesses for causing sleep issues. About 60 percent of people with HIV and more than 50 percent of people with hepatitis C experience poor sleep as do people with ME/CFS, also called chronic fatigue syndrome. People with inflammatory bowel diseaserheumatoid arthritis, and other inflammation-related diseases—all immune disorders—often suffer from lack of sleep.

Haack is investigating the details of how sleep disruption interacts with the immune system. In a study soon to be published, she and colleagues found that disturbing sleep in 24 healthy people led to the production of more molecules that prolonged inflammation and notably, a suppression of molecules that normally stop that inflammation. Even after three full nights of recovery sleep, inflammation persists, emphasizing the need to preserve good sleep in the first place.

Together, evidence illustrates that sleeplessness can cause or exacerbate many symptoms associated with both acute COVID and long COVID, including depression, fatigue, and brain fog. Those symptoms in turn can make it hard to sleep. “It’s always bi-directional,” Haack says. Insomnia, sleep apnea, and other disruptions, she says, “all can lower sleep quality, depth, continuity, or regularity, and dampen the immune supporting functions that come with normal sleep.”

Developing drugs for COVID-related sleep disorders? 

Ultimately, scientists might be able to develop medications that affect levels of cytokines to improve sleep, says James Krueger, an expert on the biochemistry of sleep at Washington State University in Spokane. But it’s a challenging task because the relationship between cytokines and sleep are extraordinarily complex. Some pro-inflammatory cytokines enhance sleep at low concentrations but at higher concentrations, they lead to wakefulness and fragmented sleep. There are also anti-inflammatory cytokines that mostly inhibit sleep at low concentrations.

Hundreds of proteins interact to regulate the immune system and other processes, Krueger says. COVID and other infections tweak those interactions. Targeting those molecules remains a work in progress. “For complex behaviors and brain processes such as sleep, some new drugs have been developed over the past few years,” he says. “Time will tell if they are better than prior drugs.”

How to improve sleep after COVID

Helping people get better rest during and after COVID infections begins with acknowledging the importance of sleep, Haack says. That can include avoiding medications that disturb sleep, such as opioids, and reducing light, noise, and repeated wakeups for people who are hospitalized.

Establishing regular sleep routines with consistent bedtimes and wakeup times are often a part of insomnia care, Axelsson says. It can also help for people to restrict time in bed to increase sleep efficiency and avoid excessive time spent lying awake.

Haack recommends mindfulness apps to reduce stress and anxiety. For her long COVID patients, Peña Orbea has seen cognitive behavioral therapy led to improvements. “With insomnia, the brain is in a hyper-arousal state,” she says. “We try to reset that arousal state of mind.”

Physical activity and fresh air can help a subset of people who may have stopped going out because of their illness, Axelsson says. But for many with long COVID, exercise can cause serious setbacks, underscoring the need for individualized medical care if sleep problems persist post-COVID.

“Sleep disruption can be quite normal during the acute COVID infection, due to sleep-disrupting symptoms such as pain, coughing, stuffy nose,” Haack says. “If sleep disturbances continue to stay beyond the acute symptomatic phase or start to develop as a new symptom, that is the time to seek help.”

Is COVID-19 Even Real?

(Update 11/11/2022)

Severe COVID could cause markers of old age in the brain

Key genes that are active in the brains of older people are also active in the brains of people who developed serious COVID-19.

(Update 12/8/2022)

Severe COVID-19 is linked to changes in the brain that mirror those seen in old age, according to an analysis of dozens of post-mortem brain samples.

The analysis revealed brain changes in gene activity that were more extensive in people who had severe SARS-CoV-2 infections than in uninfected people who had been in an intensive care unit (ICU) or had been put on ventilators to assist their breathing — treatments used in many people with serious COVID-19.

The study, published on 5 December in Nature Aging, joins a bevy of publications cataloguing the effects of COVID-19 on the brain. “It opens a plethora of questions that are important, not only for understanding the disease, but to prepare society for what the consequences of the pandemic might be,” says neuropathologist Marianna Bugiani at Amsterdam University Medical Centers. “And these consequences might not be clear for years.”

COVID on the brain

Maria Mavrikaki, a neurobiologist at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, embarked on the study about two years ago, after seeing a preprint, later published as a paper, that described cognitive decline after COVID-19. She decided to follow up to see whether she could find changes in the brain that might trigger the effects.What triggers severe COVID? Infected immune cells hold clues

She and her colleagues studied samples taken from the frontal cortex — a region of the brain closely tied to cognition — of 21 people who had severe COVID-19 when they died and one person with an asymptomatic SARS-CoV-2 infection at death. The team compared these with samples from 22 people with no known history of SARS-CoV-2 infection. Another control group comprised nine people who had no known history of infection but had spent time on a ventilator or in an ICU — interventions that can cause serious side effects.

The team found that genes associated with inflammation and stress were more active in the brains of people who had had severe COVID-19 than in the brains of people in the control group. Conversely, genes linked to cognition and the formation of connections between brain cells were less active.

The scientists also analysed brain tissue from 20 further uninfected people: 10 who were 38 years old or younger at death, and 10 who were 71 or older. A comparison revealed that people in the older group had brain changes that were similar to those seen in people with severe COVID-19.

The work is preliminary and will need to be confirmed using complementary approaches, says Daniel Martins-de-Souza, head of proteomics at the University of Campinas in Brazil. But it is an informative study, he says, and such research could ultimately guide treatment for people who have lingering cognitive difficulties after COVID-19.

Inflammatory effect

Mavrikaki suspects that COVID-19’s effects on gene activity are caused indirectly, by inflammation, rather than by viral infiltration of the brain. Supporting this interpretation, she and her colleagues found that exposing laboratory-cultured neurons to proteins that promote inflammation affected the activity of a subset of the aging-related genes.

But it’s possible that this response might also be triggered by other infections, she says. And the study could not fully control for obesity or other conditions that might both increase a person’s chances of developing severe COVID-19 and generate an inflammatory state that affects gene expression in the brain.

Another key question is whether the changes in gene expression are associated only with severe cases of COVID-19, or if milder disease can also cause them, says Bugiani. In March, a study of hundreds of brain images collected by the UK Biobank found that even mild disease could cause changes in the brain, including damage to the regions involved in smell and taste.

It will take time to determine whether the changes observed in the study are transient or are there to stay, Bugiani says. “The duration of the pandemic has now been long enough to see these things, but not long enough to establish if they are permanent,” she says. “We don’t yet know what their real consequences will be.”

Why does COVID-19 cause brain fog? Scientists may finally have an answer.

Nearly 40 percent of long COVID patients suffer from the disorienting condition. Destroyed connections between brain cells may be to blame.

(Update 12/4/2022)

When scientists at the Karolinska Institute in Sweden infected brain organoids—pinhead-size bits of brain tissue grown in the lab—with the virus that causes COVID, they found that it accelerated the destruction of connections between neurons called synapses.

The discovery adds to the growing understanding of how SARS-CoV-2 enters the central nervous system and causes disease. In the last two years, scientists have documented long-lasting neural and behavioral problems in COVID-19 patients. One such condition, known as brain fog, causes disorientation, memory loss, chronic headache, and numbness, and it affects nearly 40 percent of long COVID patients.

Carl Sellgren, a psychiatrist and cellular biologist, and his team at the Karolinska Institute decided to use the organoids to try to learn what SARS-CoV-2 does to brain and whether it might help explain the neurological symptoms.

Their research has led them to conclude that destroying too many connections between neurons, or over-pruning, may be causing brain fog in long COVID patients. “This could be one of the many reasons—probably—why we are observing a range of neurological symptoms, even after the infection is long gone,” says Samudyata, a postdoctoral researcher at Karolinska Institute who led the study and goes by one name.

Ana Osório Oliveira, a co-author and neuroscientist in Sellgren’s lab, says, “It was quite striking that very small amounts of the virus could quite rapidly spread in the organoids and eliminate an excessive number of synapses.” The research was published in the journal Molecular Psychiatry.

“This study fits in nicely with ours and several others,” says Madeline Lancaster, a neurobiologist at MRC Laboratory of Molecular Biology, Cambridge, U.K. Using brain organoids, Lancaster’s research has revealed that SARS-CoV-2 damages the protective barrier of the brain. When this barrier is breached, pathogens, aberrant immune cells, and inflammatory compounds, can enter the cerebrospinal fluid and the brain.

Pruning connections between neurons is essential for learning

The brain is made of a dense and dynamic network of nerve cells that communicate through synapses that change as humans learn. “Synapses are essentially how cells talk to each other and how information is passed from one part of the brain to another,” Lancaster says.

Synapses are responsible for all the functions of the brain, from memory to controlling movement to feeling emotions—and they are constantly remodeled. “That’s how we learn,” she says.

The junctions between neurons that talk to each other frequently have more knob-shaped ends that produce neurotransmitters—chemicals that transmit signals to other neurons—which then travel across gaps between neurons known as a synaptic cleft. Conversely, neurons that that communicate less, or not at all, have fewer synapses because they are removed, or pruned, by immune cells called microglia. Microglia make up to 17 percent of the cell population in some parts of human brain and perform housekeeping duties by migrating through the brain eating dead cells and scavenging weak synapses.

Although synaptic pruning is most active in developing brains such as in fetuses and infants, it continues in healthy brains throughout life and is necessary for encoding new memories and erasing the ones the brain no longer needs. Synaptic pruning is also critical for the brain to recover from an injury; strengthening synapses as the lost skills are relearned and removing those that no longer function.

Using brain organoids to study neural damage 

Studying a direct link between COVID-19 and cognitive dysfunction, such as brain fog, is difficult in living brains. That is why studies are often limited to cadavers of COVID-19 patients. But brain organoids, called mini-brains, allow scientists to see in real time how SARS-CoV-2 affects living tissue.

Using brain organoids, Oliveira and her colleagues found that the virus itself was not directly pruning the synaptic connections but was activating the microglia.

“We found that following infection by SARS-CoV-2, somehow the microglia become immunoreactive, and eat more of the synapses than normal,” Samudyata says.

The study is important because it clearly shows the quantitative differences in the microglial activity after COVID-19 and its effect on synapses, says Ayush Batra, a neurologist at Northwestern University Feinberg School of Medicine.

But too much synapse pruning can be detrimental and has been linked to neurodevelopmental disorders such as schizophrenia, as well as neurodegenerative conditions such as Alzheimer’s and Parkinson’s diseases.

If the excessive elimination of synapses that occurs in brain organoids after SARS-CoV-2 infection also occurs in people, it may destroy vital connections and explain why some with COVID-19 suffer from long-term neurological symptoms.

“Too much synapse elimination would be expected to affect a person’s ability to form new memories, or to remember existing ones, and could help explain the sluggish brain functions seen in brain fog,” Lancaster says.

This is consistent with studies done at the U.S. National Institutes of Health that have found antibodies produced in response to SARS-CoV-2 can attack the cells lining the brain’s blood vessels, causing damage and inflammation—which activates microglia—even if the virus doesn’t directly enter the brain. That may explain why, as Batra’s team has shown, some  long COVID patients not sick enough to be hospitalized continue to experience neurologic symptoms beyond a year after initial infection.

Is the loss of synapses causing brain shrinkage?

U.K. study has also shown that even mild COVID-19 can shrink the brain through loss of gray matter—the outermost layer of the brain that is made up of cell bodies and is vital for controlling movement, memory, and emotions—causing physical changes equivalent to a decade of aging. “We are still unclear what may contribute, in general, to a loss of gray matter volume or thickness observed using MRI,” says Gwenaëlle Douaud, a neuroscientist at the University of Oxford who led the study.

While synapse elimination, as shown in Samudyata’s study, could account for a small percentage of the change in the gray matter, says Douaud, more studies combining imaging with tissue sections are required to determine the other factors that lead to brain shrinkage.

Hyperactive microglia may cause problems in other ways. The current study also shows that the pattern of genes turned on and off by the microglia in brain organoids after SARS-CoV-2 infection mimicked gene activity seen in neurodegenerative disorders. This may explain why there is a three times higher risk of developing neurological or psychiatric conditions within six months after COVID-19 compared with those who were not infected. In adults aged over 65, the risk of developing dementia after a COVID-19 infection is almost twice that from other respiratory infections.

However, scientists caution that much more research is needed to understand the effect of SARS-CoV-2 infection on the brain. As organoids resemble immature cells—like those in a fetal or post-natal state—this limits extrapolation of the results to mature adult brain cells.

“While these data are exciting and indicate a role for proinflammatory microglia in the disease mechanisms underlying long COVID, more studies are required to validate these findings and build on them,” says Oliver Harschnitz, group leader in the Neurogenomics Research Centre at Human Technopole Institute in Milan, Italy.

It’s also not known whether long COVID has irreversible effects on the brain. So as the pace of holiday and indoor winter activities picks up, Samudyata advises taking preventative measures and staying up to date on vaccinations to minimize the chance of getting COVID over and over. While it isn’t clear how the virus exerts detrimental effects on the brain, it’s evident that it does cause damage.

How do you know if you have long COVID?

There is no single diagnostic test for it, and no medical consensus about what symptoms it encompasses. Experts weigh in on what you can do if you still feel sick.

(Update 12/16/2022)

A few days after Michele Hart tested negative following a COVID infection in June 2022, she started participating in virtual meetings for her job. But after each call, she crawled back into bed to rest. When she returned home from a three-day work trip, more than a week after her negative test, she spent the entire weekend in bed recovering. An avid runner and hiker, she had stopped doing both because she was tired and, she thought, possibly depressed. She wondered if she would ever feel well again.

“One of the things I found myself doing after that initial 10 days was, at least once a day, Googling something like, ‘When will I be better?’” says Hart, 45, a product specialist for a school curriculum company. The answers were frustrating: “Hang in there. Some people have it like this. Some people have it like that.”

Long Covid patient waiting for exam.
A long COVID patient began her day waiting in the exam room for the first of four doctor appointments. An active athlete, since having long COVID she gets fatigued more easily. She had to reteach herself how to dribble a basketball.PHOTOGRAPH BY JACKIE MOLLOY

COVID symptoms often don’t end when people test negative, which usually happens after about 10 days. Symptoms can last for weeks, months, or more. In one of the latest studies on lingering symptoms, researchers in Scotland surveyed more than 31,000 people who’d had symptomatic infections and found that 42 percent reported they had not fully recovered between six and 18 months after their infection began.

But when do ongoing COVID symptoms officially become long COVID, and how can someone know if they have a chronic condition or symptoms that will go away eventually?

Those are tricky questions without satisfying answers, says Michael VanElzakker, a neuroscientist at Harvard Medical School and Massachusetts General Hospital. Long COVID, while an active area of research, is not a clearly defined condition with specific medical criteria. There is no single diagnostic test to confirm it and no easy way to explain what is causing symptoms. Many studies are ongoing, but answers are still a work in progress.

“A core question still remains,” VanElzakker says. “Why do some people seem to fully recover, and some don’t?”

What is long COVID?

There is still no medical consensus about what the condition should be called, which symptoms it encompasses, how long a person must be sick before being diagnosed with it, or exactly how many people experience it.

Symptoms need to persist for at least three months after a probable or confirmed COVID infection to meet the World Health Organization’s definition of a post-COVID condition. The U.S. Centers for Disease Control and Prevention considers four weeks long enough to suspect long COVID, which is also called post-acute sequelae of SARS CoV-2 infection (PASC), long-haul COVID, chronic COVID, and other names.

After multiple large studies it still isn’t clear how many people are suffering from long-term symptoms, which are wide ranging. A study conducted in Germany identified 96 potential symptoms and found many of them in people who’d had prior infections. For young people, the most common symptoms included fatigue, cough, throat and chest pain, headache, fever, abdominal pain, anxiety, and depression. For adults, frequent ongoing symptoms included changes to smell and taste, fever, trouble breathing, coughing, throat and chest pain, hair loss, fatigue, exhaustion, and headache.

The Scottish study considered 26 persistent symptoms, including headaches, loss of taste and smell, tiredness, heart palpitations, constipation, breathlessness, joint pain, dizziness, and depression. But complicating the issue of diagnosis was that people who hadn’t tested positive for COVID also experienced many of those same symptoms.

While 42 percent of people in the Scottish study had some lingering symptoms, an additional 6 percent said they hadn’t recovered at all. German researchers found that adults, kids, and adolescents with a prior COVID infection were about 30 percent more likely than people without a positive COVID test to report a new condition more than three months after their infection. About 14 percent of more than 41,000 of people who responded to a CDC survey in October reported having persistent symptoms at least three months after a COVID infection.

Across studies, it looks like somewhere between one in five and one in 20 people end up with long COVID symptoms, says David Putrino, a neuroscientist at Mount Sinai Health System in New York. To him, the exact number is less important than the reality of the implications. “If any of those are true, it’s an enormous number,” he says. “My clinic already has a six-month waitlist crammed out the door. None of us are sleeping. We’re all just treating 24/7.”

Will I get better?

Also unclear is the prognosis for people with lingering symptoms. Most patients who visit Mount Sinai’s Center for Post-COVID Care show some improvement within the first three months of rehab even if they experience setbacks or don’t feel fully recovered, Putrino says. But about 10 percent don’t improve.

Some might ultimately meet the criteria for myalgic encephalomyelitis or chronic fatigue syndrome, known shorthand as ME/CFS, a chronic condition that can be caused by viral infections. About 10 percent of people with severe cases of Epstein-Barr go on to develop ME/CFS, VanElzakker says. He suspects this will happen to a subset of long COVID patients.

On the flip side are people with lingering issues that ultimately go away, says VanElzakker, who lost patches of hair from his beard for several months after his own bouts with the virus. “Simply because someone doesn’t feel better after three weeks,” he says, “doesn’t mean they’re never going to get better.”

What is causing it?

For people with ongoing symptoms, there are many potential causes, experts say, and understanding them can help guide treatment. One active area of research suggests that SARS-CoV-2, the virus that causes COVID-19, might stick around in some people’s bodies, driving inflammation and symptoms long after rapid COVID tests come up negative. In a study of 44 people who died from or with COVID in 2020 and 2021, researchers found evidence of the SARS-CoV-2 spike protein in organs including the brain, heart, and intestines that had persisted for as long as seven months, even in people who were asymptomatic. The virus replicated within tissues for up to three months in some people, the study found.

Viral reservoirs are hard to detect in living patients because they don’t show up in blood tests, VanElzakker says. He has co-founded a nonprofit called Polybio to investigate infection-associated chronic conditions like long COVID. The organization is funding research to collect gut samples from long COVID patients, and another that will collect lung tissue. He suspects that identifying where the virus ends up settling could explain the wide range of long COVID symptoms. If reservoirs get established in the gut, they could cause ongoing diarrhea, for example. In the lungs, they could cause coughing and shortness of breath.

As researchers compile evidence for viral reservoirs and other possible causes of long-term symptoms, the work is starting to guide treatment that recognizes the importance of individualized care, Putrino says. A patient with lingering symptoms from severe pneumonia and intubation, for instance, might benefit from pulmonary rehabilitation that pushes them to exert themselves. But the same kind of rehab can be disastrous for someone with post-exertional malaise who meets the criteria for ME/CFS. Antivirals might end up helping people with persistent reservoirs of COVID, but it doesn’t make sense to give these drugs to everyone with long COVID.

“Our job now is to understand who’s who in this big broad diagnostic catchall,” Putrino says, “so that we can start to engage in precision medicine.”

What should I do if I still feel sick? 

If symptoms persist beyond four weeks, it’s probably time to talk with your doctor about checking your heart and lungs and running other basic tests, Putrino says. If you get to 12 weeks, he recommends a more aggressive approach with a physician or high-quality clinic that is familiar with long COVID.

Because the pandemic has been such a difficult time in so many ways, a careful check of both physical and mental health can start to distinguish between the mix of problems people might be experiencing right now, says Lucinda Bateman, medical director of the Bateman Horn Center, a nonprofit focused on research into ME/CFS, fibromyalgia, and related conditions.

Some health issues that started after a COVID infection may be related to the severe stress of living through a pandemic or to missed medical appointments due to lockdowns, clinic closures, and overbooked doctors.

For people who have been to general practitioners and specialists and still don’t have an answer, clinicians knowledgeable about ME/CFS could be helpful. They might look for signs of mast cell activation, a type of hyper-inflammation, Bateman says. Or they might consider dysautonomia, which is dysfunction of the autonomic nervous system that can be detected by looking for a drop in blood pressure or spike in heart rate when standing up. These conditions are tricky to diagnose because they can affect multiple systems and produce symptoms throughout the body, but distinctions can make a difference in medical guidance.

People don’t usually get diagnosed with ME/CFS until they have been sick for between two and five years presumably, Bateman says, because doctors have not been taught about the illness. One hope is that, with an emerging cohort of long COVID patients, clinicians might be able to catch cases earlier and prevent them from progressing—by, for example, limiting physical and even cognitive activity during recovery for some people. “We’re a culture of high-achieving and of pushing through pain, and that’s the wrong advice for some conditions,” she says, “particularly for post-viral conditions that relapse with activity.”

As for Hart, her turning point came on the Fourth of July, after about a month of being sick, when she went to a concert and found that she was able to dance. There were ups and down for a couple of weeks after that, but now, six months later, she is back to full speed. “I couldn’t do anything for like six weeks,” she says. “But then I was fine.”

Omicron variant XBB.1.5 is the most contagious yet

(Update 1/11/2023)

A highly contagious subvariant of Omicron called XBB.1.5 is now the dominant strain spreading in the United States. Early data suggests it’s more evasive than other variants, efficiently dodging previously acquired immunity and raising concerns among public health officials about a possible winter wave.

In December alone, XBB.1.5 grew from causing fewer than 1 percent of confirmed COVID-19 cases nationwide to more than 40 percent, rapidly out-competing other variants. In northeastern states it caused more than 75 percent of all cases for the week beginning December 25, although there is no data yet to indicate whether it causes more severe disease.

“It is the most transmissible subvariant that has been detected yet,” said Maria Van Kerkhove, the technical lead for COVID-19 response at the World Health Organization, during a news conference. Scientists estimate that someone infected with XBB.1.5 can cause 60 percent more infections than a person infected with its parent strains. 

XBB.1.5 was first detected in New York and Connecticut in late October but has since been detected in at least 29 other countries. While it accounts for less than 5 percent of current cases worldwide, it seems to be doubling within eight to 15 days, making it the fastest-spreading SARS-CoV-2 variant to date. In fact, XBB.1.5 might be far more widespread, according to Kerkhove, since it’s difficult to tell as genomic sequencing efforts for monitoring the SARS-CoV-2 have declined around the world.

Where did XBB.1.5 come from?

XBB.1.5 descended from variant XBB.1, which arose from XBB—the fusion of two Omicron BA.2 variants. Its grandparental strain, XBB, and its parental strain XBB.1—responsible for a surge of COVID-19 cases in parts of Asia in October and November 2022—were able to evade immunity conferred by previous infections and the bivalent boosters that were specifically designed to block Omicron variants, according to a report published in Nature in December. In Singapore, XBB subvariants caused a large number of breakthrough infections and reinfections, although hospitalization rates remained low.

How is the new variant different?

The XBB.1.5 variant features a new mutation at the 486 position of the spike, which is the protein the virus uses to bind to the ACE2 receptor protein on cells in the human respiratory tract. Mathematical models predicted that a change in the spike protein at this position would allow a variant to escape previous antibodies. Those predictions seem to be correct.

“The mutation brings higher ACE2 binding while maintaining XBB.1’s extremely high immune evasion capability,” says Yunlong Cao, of Peking University in China, based on his preliminary research exploring the enhanced contagiousness of XBB.1.5, which is not yet peer reviewed.

Cao’s preliminary research also shows that some monoclonal antibody therapies, such as Evusheld and Bebtelovimab, do not block XBB.1.5, although Sotrovimab provided weak protection.

Does the bivalent booster protect against XBB.1.5?

It’s too early to know how the current bivalent booster—which targets previous Omicron strains BA.4 and BA.5, as well as the original coronavirus would protect against XBB.1.5. However, recent research on the parental strains of XBB.1.5 led by Mehul Suthar, an immunologist at Emory University School of Medicine, shows that people who got the bivalent booster, as well as those who were recently infected with an Omicron variant, had slightly higher levels of protective antibodies.

“Bivalent boosters seem to be working the way they are supposed to,” says Suthar, by shifting our immunity towards Omicron variants. He speculates that the bivalent booster would provide some protection against XBB.1.5, based on its similarity to other Omicron variants. But his research also suggests that even the bivalent booster may not block XBB.1.5 breakthrough infections.

The Centers for Disease Control and Prevention estimates that bivalent boosters reduced COVID-19 hospitalizations by more than 90 percent through November, which is the latest data available. This means even if the boosters may not prevent infections, they may still save lives.

“It is difficult to say anything about pathogenicity of XBB.1.5 yet,” says Kei Sato, a virologist at the University of Tokyo, since there are no data yet. However, Sato’s preliminary work, not yet peer reviewed, on parent strain XBB has shown that the virus attaches more tightly to human cells than other Omicron variants, such as BA.2.75 and BA.2, which suggests it might cause more severe disease. But when hamsters were infected with XBB, the disease symptoms were no worse than those caused by BA.2.75. “We do not have any ideas explaining this discrepancy yet,” says Sato.

Will XBB.1.5 drag out the pandemic?

Hospitalizations due to COVID-19 have risen by 17 percent in the last week, according to the latest CDC data, leading scientists to worry that even without causing more serious disease, a highly contagious XBB.1.5 could worsen the course of the now three-year-long pandemic. Large number of COVID-19 cases can still overwhelm hospitals, where resources are already stretched thin with the high number of RSV and flu respiratory infections.

People ages 65 and older are the most vulnerable to the complications due to COVID-19. Yet, just slightly more than a third of these Americans have received the bivalent booster, leaving them vulnerable to XBB.1.5. When it comes to the U.S. population, nearly 85 percent of those eligible have not received the bivalent shot.

“When infections are high, many people will be affected,” says Marc Veldhoen, an immunologist at the Institute of Molecular Medicine in Lisbon, Portugal. “More infections hold more risk, more likelihood of symptoms, and unfortunately, high circulation means many vulnerable [people] will be infected and we will see more people in hospitals.”

CDC Investigating Possible Link Between COVID Vaccine and Increased Risk of Stroke

(Update 1/14/2023)

The Centers for Disease Control and Prevention has gently dipped its official toe into concerns that there could be a link between COVID-19 vaccines and strokes.

statement released Friday by the CDC concerning the Pfizer-BioNTech vaccine said the possibility exists of a link between the bivalent form of the vaccine and stroke, all the while insisting that Americans should be vaccinated.

So what is a bivalent vaccine? “The bivalent COVID-19 vaccines include a component of the original virus strain to provide broad protection against COVID-19 and a component of the omicron variant to provide better protection against COVID-19 caused by the omicron variant,” the FDA says on its website.

The FDA said the bivalent Pfizer vaccine is used as a booster for those who have had their initial vaccinations.

The CDC release said that the U.S. government has “safety monitoring systems” in place to detect “possible safety signals for vaccines.”

In this case, the release said, the CDC’s Vaccine Safety Datalink prompted agencies to launch an investigation into Pfizer-BioNTech’s bivalent COVID-19 vaccine.

The issue, it said, is “a safety concern for ischemic stroke in people ages 65 and older who received the Pfizer-BioNTech COVID-19 Vaccine, Bivalent.”

“Rapid-response investigation of the signal in the VSD raised a question of whether people 65 and older who have received the Pfizer-BioNTech COVID-19 Vaccine, Bivalent were more likely to have an ischemic stroke in the 21 days following vaccination compared with days 22-44 following vaccination,” the CDC release said.

The release said no such issue had been found with the Moderna bivalent vaccine. It cautioned that “these safety systems detect signals that could be due to factors other than the vaccine itself” and said no other monitoring system had raised the alarm.

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The agency added that various studies using Medicaid and Veterans Affairs databases have shown no such concern, nor has research in other countries.

“Although the totality of the data currently suggests that it is very unlikely that the signal in VSD represents a true clinical risk, we believe it is important to share this information with the public,” the CDC said, adding that “no change in vaccination practice is recommended.”

Pfizer offered a statement in reply to the CDC, according to Fox News.

“Pfizer and BioNTech have been made aware of limited reports of ischemic stroke that have been observed in the CDC Vaccine Safety DataLink (VSD) database in people 65 and older following vaccination with the Omicron BA.4/BA.5-adapted bivalent COVID-19 Vaccine by Pfizer and BioNTech.”

“Neither Pfizer and BioNTech nor the CDC or the U.S. Food and Drug Administration (FDA) have observed similar findings across numerous other monitoring systems in the U.S. and globally and there is no evidence to conclude that ischemic stroke is associated with the use of the companies’ COVID-19 vaccines,” the statement said.

“Compared to published incidence rates of ischemic stroke in this older population, the companies to date have observed a lower number of reported ischemic strokes following the vaccination with the Omicron BA.4/BA.5-adapted bivalent vaccine.”

Dr. Marc Siegel, a Fox News medical contributor, said the CDC’s release is not proof of a link between the vaccine and strokes.

“This is not proof. This is that they see there may be a link here, and they want to investigate it, and they’re trying to be transparent,” he said.

Republican Washington Rep. Cathy McMorris Rodgers called for the CDC and FDA to “rapidly investigate, in an open and transparent manner, whether or not the vaccine may have contributed to the reported strokes,” according to Politico.

“If there’s one lesson that the CDC and FDA should have taken away from the pandemic, it’s the importance of providing honest, clear, precise, and timely information to the American people about the potential risks and benefits of COVID-19 interventions, including vaccination,” she said.

COVID-19 Leads to an Alarming Rise in Heart Attacks

(Update 1/20/2023)

Top Expert Sounds the Alarm, Calls for Immediate Suspension of All mRNA Vaccines

(Update 2/2/2023)

Retsef Levi, an expert in risk management relating to the health field, is calling for the immediate suspension of all COVID-19 messenger RNA vaccines.

After performing a risk analysis of the vaccines, Levi — a professor in the Massachusetts Institute of Technology’s Sloan School of Management — revealed his recommendation and supporting evidence in a video posted to Twitter on Sunday.

As of Monday afternoon, the video had more than 1.1 million views.

“I’m filming this video to share my strong conviction that at this point in time, all COVID mRNA vaccination program[s] should stop immediately,” Levi said.

He said he believes the vaccines have “completely failed” to live up to the promises of efficacy given by health officials and vaccine manufacturers.

Furthermore, Levi asserted there was “mounting and indisputable” evidence that the vaccines cause an “unprecedented level of harm,” including the deaths of young people.

For example, shortly after the vaccines were introduced to the public, the Johnson & Johnson and AstraZeneca shots were found to cause vaccine-induced immune thrombotic thrombocytopenia, a blood-clotting condition, in roughly 1 in 26,000 to 1 in 127,000 people, most of whom were young women.

Most public concern over the vaccines, however, comes from another rare yet serious side effect found in the Moderna and Pfizer mRNA vaccines: myocarditis. These side effects are found most often in young adult and adolescent males, according to the Centers for Disease Control and Prevention.

Some experts believe the severity of these side effects has been downplayed by health authorities.

“We think the vaccines are an important tool for preventing severe illness and death among vulnerable people … But we have been concerned that our federal officials recklessly continue to push for multiple Covid shots for everyone five years old and up, despite the growing evidence that these vaccines may not be appropriate for all,” Drs. Vinay Prasad and John Mandrola wrote in a Wednesday article for The Free Press, an outlet founded by journalist Bari Weiss.

“We are also concerned about the way side effects of the vaccine, particularly among young men, have been downplayed,” they wrote.

In a report released on Nov. 7, the American College of Cardiology estimated the myocarditis complication rate to be 35.6 cases per million doses for the Moderna vaccine and 12.6 per million for the Pfizer vaccine. In 2018, before the vaccines, there were about 2 cases of myocarditis per million people under age 40 and 2.2 per million over 40, the report said.

According to Levi, vaccine side effects are likely more common than studies currently show. In his view, this is because cases of myocarditis are severely underreported and undetected.

“Since myocarditis is known to be hard to diagnose … I was very concerned that it will not be detected by the existing vaccine safety surveillance systems,” he explained in the video.

After performing an analysis of data from Israel’s emergency medical services, Levi found some “very concerning signals,” he said.

Comparing data from 2019 to the first half of 2021, Levi and his fellow researchers found a 25 percent increase in cases of cardiac arrest in people ages 16 to 39.

He also said he found a correlation between this increase and the same population receiving Pfizer vaccine doses.

Over the same time period, Levi’s research found no correlation between the increase in cardiac events and COVID-19 infections.

“While this is not proof of [a] casual relationship, it left us very concerned, especially given the known suspect clinical mechanism,” Levi said in the video.

Despite calling for an investigation into the “causal mechanisms” of the increase in deaths, he said that, “to the best of my knowledge,” no such investigation has been conducted.

“I think there is no other ethical or scientific choice but to pull out of the market these medical products and stop all the mRNA vaccination programs,” Levi said.

“This is clearly the most failing medical product in the history of medical products, both in terms of efficacy and safety,” he concluded.

COVID drug drives viral mutations — and now some want to halt its use

Analysis reveals the signature of the antiviral drug molnupiravir in SARS-CoV-2 sequences riddled with mutations.

(Update 2/8/2023

A drug widely used to treat COVID-19 might be spurring the evolution of new SARS-CoV-2 variants.

The drug, molnupiravir, works by introducing a flurry of mutations to the viral genome; this helps to clear infections. But a study of more than 13 million SARS-CoV-2 sequences has uncovered sequences that bear molnupiravir’s fingerprints. The study’s authors say the results suggest that molnupiravir treatment has sparked the evolution of viral lineages carrying numerous mutations that, in at least some cases, have the capacity to spread to other individuals.

The study was posted on the medRxiv preprint server in January. It has not yet been peer reviewed.

“Whether this should be of concern — that is an open question,” says Jesse Bloom, an evolutionary virologist at the Fred Hutchinson Cancer Research Center in Seattle, Washington. Mutations to the SARS-CoV-2 genome can help the virus to evade immunity and become more transmissible, but most mutations are likely to harm it.

Molecular mimic

Molnupiravir was developed by the pharmaceutical giant Merck, based in Rahway, New Jersey, and was authorized by regulators in the United States and United Kingdom in late 2021, and in Australia in early 2022. A company-sponsored clinical trial found that the drug — a pill taken for five days — reduced hospitalizations and deaths in people at risk of severe COVID-19.

Molnupiravir mimics some of the building blocks of RNA, the genetic material in SARS-CoV-2. The drug peppers the viral genome with mutations, which add up to make SARS-CoV-2 worse at replicating. This results in a marked reduction in SARS-CoV-2 levels in infected human cells and hamsters.

But scientists have raised the possibility that, in rare cases, molnupiravir treatment might not entirely eliminate SARS-CoV-2, allowing some individuals who have taken the drug to continue to to transmit the virus.

Those concerns were largely theoretical, until Ryan Hisner, a US schoolteacher who is part of a loose-knit community of SARS-CoV-2 variant spotters, started noticing peculiar patterns in sequencing data from around the world: a number of lineages carried many more mutations than their nearest relatives. Most of the genetic changes were of the type induced by molnupiravir.

The researchers’ analysis of global sequences showed that the prevalence of the suspect lineages rose substantially in 2022, the first year molnupiravir was widely used. The lineages were also much more likely to show up in sequencing data from countries where the drug was used — the United States, the United Kingdom and Australia — than in data from countries that hadn’t approved it, such as France and Canada.

Where SARS-CoV-2 sequence data include the age of the individual sampled, the telltale lineages tended to have come from older people, who are more likely to take molnupiravir. And in Australia, where molnupiravir was pre-placed in care homes, the researchers identified a viral lineage carrying 25 mutations that had infected at least 20 people, mostly in their eighties and nineties.

Among the lineages that showed molnupiravir’s influence, a few — including the one from Australia — were represented by multiple sequences, indicating that they were capable of spreading. “I would say that our work closes down the possibility that these viruses can never be transmitted,” says team member Theo Sanderson, a computational biologist at the Francis Crick Institute in London.

Evolutionary dead ends?

Evidence linking molnupiravir to the mutation-heavy sequences is “circumstantial”, Merck said in a statement. “The authors assume these mutations were associated with molnupiravir treatment without evidence the viral sequences were isolated from treated patients.”

Bloom thinks the researchers make a good case that molnupiravir treatment is yielding some highly mutated viruses with the capacity to spread. But it’s not clear whether this could contribute to new coronavirus variants, or whether it is simply creating weakling viruses that are unlikely to spread very far. “SARS-CoV-2 is already generating plenty of mutations even in the absence of drug treatment,” he adds.

Rustem Ismagilov, a quantitative bioscientist at the California Institute of Technology in Pasadena, says the study underscores the need to quickly measure any risk that molnupiravir poses to sparking new variants and weigh them against the drug’s benefits. “If we are playing Russian roulette, we’d better know our odds.”

Sarah Otto, an evolutionary biologist at the University of British Columbia in Vancouver, Canada, says the paper is another blow to the continued use of molnupiravir. She notes that a large-scale UK study found that the drug had no effect on hospitalizations or deaths. “Given the large-scale risks of this mutagen producing new variants faster, including variants that are immune evasive, I encourage public-health leaders to call for a global halt to its use,” Otto says.

WHO abandons plans for crucial second phase of COVID-origins investigation

(Update 2/16/2023)

The World Health Organization (WHO) has quietly shelved the second phase of its much-anticipated scientific investigation into the origins of the COVID-19 pandemic, citing ongoing challenges over attempts to conduct crucial studies in China, Nature has learned.

Researchers say they are disappointed that the investigation isn’t going ahead, because understanding how the coronavirus SARS-CoV-2 first infected people is important for preventing future outbreaks. But without access to China, there is little that the WHO can do to advance the studies, says Angela Rasmussen, a virologist at the University of Saskatchewan in Saskatoon, Canada. “Their hands are really tied.”

In January 2021, an international team of experts convened by the WHO travelled to Wuhan, China, where the virus that causes COVID-19 was first detected. Together with Chinese researchers, the team reviewed evidence on when and how the virus might have emerged, as part of phase one. The team released a report in March that year outlining four possible scenarios, the most likely being that SARS-CoV-2 spread from bats to people, possibly through an intermediate species. Phase one was designed to lay the groundwork for a second phase of in-depth studies to pin down exactly what happened in China and elsewhere.

But two years since that high-profile trip, the WHO has abandoned its phase-two plans. “There is no phase two,” Maria Van Kerkhove, an epidemiologist at the WHO in Geneva, Switzerland, told Nature. The WHO planned for work to be done in phases, she said, but “that plan has changed”. “The politics across the world of this really hampered progress on understanding the origins,” she said.

Researchers are undertaking some work to pin down a timeline of the virus’s initial spread. This includes efforts to trap bats in regions bordering China in search of viruses closely related to SARS-CoV-2; experimental studies to help narrow down which animals are susceptible to the virus and could be hosts; and testing of archived wastewater and blood samples collected around the world in late 2019 and early 2020. But researchers say that too much time has passed to gather some of the data needed to pinpoint where the virus originated.

Tense times

Many researchers aren’t surprised the WHO’s plans have been thwarted. In early 2020, members of then US president Donald Trump’s administration made unsubstantiated claims that the virus had originated in a Chinese laboratory, and US intelligence officials later said they had begun investigations. The city of Wuhan is home to the Wuhan Institute of Virology, a high-security lab that works on coronaviruses. Chinese officials questioned whether the virus originated inside the country’s borders.

Amid simmering hostility between the two superpowers, WHO member states requested in May 2020 that the agency put together a science-led effort to identify how the pandemic started. Although China agreed to the mission, tensions were high by the time the WHO group left for Wuhan, and engagement with China quickly unravelled after the group returned.

In its March 2021 report, the team concluded that it was “extremely unlikely” that the virus had accidentally escaped from a laboratory. But the inclusion of the lab-incident scenario in the final report was a key point of contention for Chinese researchers and officials, says Dominic Dwyer, a virologist at New South Wales Health Pathology in Sydney, who was a member of the WHO team.

That July, the WHO sent a circular to member states outlining how it planned to advance origins studies. Proposed steps included assessing wild-animal markets in and around Wuhan and the farms that supplied those markets, as well as audits of labs in the area where the first cases were identified.

But Chinese officials rejected the WHO’s plans, taking particular issue with the proposal to investigate lab breaches. Zhao Lijian, the spokesperson for China’s foreign ministry, said the WHO proposal was not agreed by all member states, and that the second phase should not focus on pathways the mission report had already deemed extremely unlikely.

In August 2021, members of the original mission team published a Comment piece in Nature urging quick action on the proposed studies to trace the virus’s origins. “We wrote that piece because we were worried phase two might not happen,” says Marion Koopmans, a virologist at Erasmus University Medical Center in Rotterdam, the Netherlands, and a member of the mission to Wuhan. “I’m sorry to say that that’s indeed what panned out.”

Stalled work

Gerald Keusch, associate director of the National Emerging Infectious Diseases Laboratory Institute at Boston University in Massachusetts, says the origins investigation was “poorly handled by the global community. It was poorly handled by China. It was poorly handled by the WHO.” The WHO should have been relentless in creating a positive working relationship with the Chinese authorities, says Keusch; if it was being stonewalled, it should have been honest about that.

Van Kerkhove says that the WHO’s director-general, Tedros Adhanom Ghebreyesus, has continued to engage directly with Chinese government officials to encourage China to be more open and to share data. And WHO staff have reached out to the China Center for Disease Control and Prevention in Beijing to try to establish collaborations. “We really, really want to be able to work with our colleagues there,” says Van Kerkhove. “It’s really a deep frustration.”

The Chinese ministry of foreign affairs did not respond to Nature’s e-mailed requests for comment on why the phase-two studies have stalled.

In November 2021, the WHO formed the Scientific Advisory Group for the Origins of Novel Pathogens (SAGO) — a permanent team of experts who have since written a proposal for how to conduct origins studies for future outbreaks. SAGO has also evaluated evidence on the origins of SARS-CoV-2.

Blood-donors study

Outside the formal WHO-led process, some studies proposed for phase two have gone ahead. In May last year, researchers in Beijing and Wuhan published the results of an analysis of donor blood supplied to the Wuhan Blood Center before December 2019. The researchers were looking for SARS-CoV-2 antibodies that could signify some of the earliest infections in the pandemic. The team screened more than 88,000 plasma samples collected between 1 September and 31 December 2019, but did not find any SARS-CoV-2-blocking antibodies in the samples.

Michael Worobey, an evolutionary virologist at the University of Arizona in Tucson, says the work is an important contribution from Chinese scientists, supporting earlier genomic analyses showing that the virus probably had not emerged as early as September and was not widespread in Wuhan in late 2019.

Another study by researchers from China, which has not been peer reviewed, reported finding traces of SARS-CoV-2 in January and February 2020 at the Huanan seafood market in Wuhan, which was visited by many of the earliest known people with COVID-19. Samples were taken from sewage, drains, the surfaces of doors and market stalls, and the ground, among other places. The researchers concluded that the virus was probably shed by humans, but Rasmussen and others are keen to take a closer look at the raw data, which included swabs from a defeathering machine, to see whether they can identify animal species.

“I still hope that progress will be made,” says Thea Fischer, a public-health virologist at the University of Copenhagen, who was a member of the mission to Wuhan and is part of SAGO.

COVID-origins study links raccoon dogs to Wuhan market: what scientists think

Some scientists say the analysis provides new evidence supporting the hypothesis that the virus that causes COVID-19 spilled over from an animal — but falls short of definitive proof.

(Update 3/22/2023)

Raccoon dogs, bamboo rats, palm civets: these are just some of the animals whose DNA has been found in swabs taken from the Huanan Seafood Wholesale Market in Wuhan, China, which has been linked to the origin of the COVID-19 pandemic. The swabs also tested positive for SARS-CoV-2, which causes the disease. The analysis — posted on 20 March to the research repository Zenodo — provides evidence supporting the hypothesis that SARS-CoV-2 spilled over from animals to humans at the market, say some researchers.

“Of course, this is not direct evidence,” says Leo Poon, a virologist at the University of Hong Kong, “but this is the best we can get now, because all the animals have been eliminated from the market and we don’t have swabs of the animals.”

On 16 March, The Atlantic first reported on the analysis. The Zenodo posting, which has not been peer reviewed, is the first time that the full work has been released publicly — which could pave the way for follow-up studies, such as an investigation of where the animals in the market came from.

The swabs were collected in early 2020, after the market was shut down and cleared of animal products.

The researchers were specifically interested in looking for evidence of mammals, which could have been intermediate hosts of the virus. They identified near-complete mitochondrial DNA sequences — some 16,000-base-pairs long — for five species of wildlife, including raccoon dog (Nyctereutes procyonoides), Malayan porcupine (Hystrix brachyura), Amur hedgehog (Erinaceus amurensis), masked palm civet (Paguma larvata) and hoary bamboo rat (Rhizomys pruinosus). “It’s remarkable to have a list,” says study co-author Alex Crits-Christoph, who is a computational biologist at a non-profit organization, and is based in Baltimore, Maryland.

Particularly notable was the raccoon dog mitochondrial DNA found in six samples from two stalls. Research has shown that raccoon dogs — small fox-like animals — are susceptible to SARS-CoV-2, and can spread the infection to other raccoon dogs without showing clear signs of sickness. Raccoon dogs and masked palm civets have also been found with infections of viruses that are almost identical to the one that causes severe acute respiratory syndrome (SARS), which is related to SARS-CoV-2 and caused an outbreak in people in 2003. And work in palm-civet cells indicates that the creatures could possibly become infected with SARS-CoV-2.

Studies suggest that a progenitor of SARS-CoV-2 probably originated in bats, but how it passed from bats to people is not clear. Scientists suspect an intermediate host was involved, but they have not found strong evidence, which has led to speculation that the virus could have instead leaked — deliberately or accidentally — from a laboratory in Wuhan.

The new study does not confirm whether the animals themselves were infected with the virus. But establishing that the animals were present at the market supports the hypothesis that the pandemic had an animal origin, say some researchers.

The information could be used to track where the animals in the market came from, which could inform efforts to understand the pandemic’s start.

Others are more cautious about drawing conclusions on the origins of the pandemic from the analysis. The work confirms which animal species were at the market, but because it includes only samples that had tested positive, “there is no data in this work associating SARS-CoV-2 with the presence of any of these animals”, says Justin Kinney, a quantitative biologist at Cold Spring Harbor Laboratory in New York.

“These data do not provide a definitive answer to the question of how the pandemic began,” said Tedros Adhanom Ghebreyesus, director-general of the World Health Organization (WHO), at a press event on 17 March, after he had been briefed in advance of the report’s release. “But every piece of data is important in moving us closer to that answer,” he said.

Appearance and disappearance

The swabs were originally referred to in a preprint paper by George Gao, former director of the Chinese Center for Disease Control (China CDC) and colleagues, posted on Research Square in February 2022. Researchers have asked for that data to be made public on several occasions, without success.

But Florence Débarre, an evolutionary biologist at the French National Centre for Scientific Research, who is also a co-author on the latest report, discovered the data almost by chance on the public data repository GISAID on 4 March. “Basically, [they’re] the ones we’ve been waiting for, for a year,” she says.

In total, Débarre and her colleagues downloaded around half a terabyte of genomic data from some 50 samples. The data included almost all the swabs taken from drains, market stalls and the ground between January and February 2020 that had tested positive for SARS-CoV-2. “We’re talking about millions and millions of sequencing reads,” says Crits-Christoph.

But soon after the researchers downloaded the data, it disappeared from public view on GISAID.

A spokesperson for GISAID told Nature in an e-mail that it does not delete records, but that contributors often update their records, and, during that time, records “become temporarily invisible”. The market-swab data “are currently being updated with newer and additional data as part of a manuscript currently under review”. (The Gao paper is marked as ‘under review’ at Nature Portfolio Nature’s news team is independent of its publisher Springer Nature, which publishes Nature Portfolio.)

Débarre and her colleagues say they reached out to authors of the preprint to collaborate on the analysis, but the China CDC declined. On 14 March, her colleagues, as well as members of the China CDC, presented their work to the WHO at a meeting of the Scientific Advisory Group for the Origins of Novel Pathogens, a body tasked with investigating outbreaks, including the origins of SARS-CoV-2.

At the WHO press briefing on 17 March, Tedros called on the China CDC researchers to be transparent in sharing data. “These data could have and should have been shared three years ago,” he said.

Gao did not respond to Nature’s requests for comment.

Débarre recognizes that it has taken a long time to share this data, but acknowledges the environmental sampling and sequencing work conducted by the China CDC. “They did what needed to be done,” she says. “We wouldn’t have this data, if it wasn’t for their work.”

Wild match

Previous studies have found that Chinese bamboo rats (Rhizomys sinensis) and raccoon dogs were sold at the Huanan market between May 2017 and November 2019, and that several stalls were probably selling live or freshly killed mammals or other meat products. The data confirm that “exactly what we thought was there in the market, was there in the market”, says Joel Wertheim, a molecular epidemiologist at the University of California, San Diego, and another co-author of the analysis.

The area where most of the SARS-CoV-2-positive samples clustered was also where most of the samples containing wild-animal DNA were found, which Poon says “agrees with the hypothesis that maybe the virus came from animals”. Positive swabs from the eastern section of the market primarily contained human DNA — suggesting that there was some human-to-human transmission at the market in early 2020, says Poon.

In one sample from a cart used to move cages, the researchers found RNA and DNA that matched the raccoon-dog genome, and very little that matched the human genome. “The most logical hypothesis is that raccoon dogs were infected by SARS-CoV-2 and shed the virus,” says Poon.

But it is possible that the site was contaminated with SARS-CoV-2 RNA from other sources. “There is no evidence that the virus came from an infected raccoon dog; it could just as easily have come from an infected person,” says Kinney.

More data

Many more forensic insights could still come from the data if they were made public again, says Crits-Christoph. For example, by looking at the ratio of RNA to DNA for different animal species, researchers could determine how recently those animals were present at the market, because DNA typically persists in the environment longer than RNA does. But more details are needed about how the samples were collected, processed and sequenced, says Wertheim.

A close study of the RNA data could possibly determine whether the animals at the market were sick, adds Crits-Christoph. Does it seem like the creatures were in “a disease state, or a healthy state?” he asks. “There’s all sorts of wonderful, complex questions in the data.”

There are more data that have not yet been shared — including environmental swabs that were negative for SARS-CoV-2, and detailed virus data. Those data are important to analyse, to get a better picture of what was happening at the market, says Wertheim.

COVID-origins data from Wuhan market published: what scientists think

First peer-reviewed analysis of the Chinese swabs confirms animal DNA was present in samples that tested positive for SARS-CoV-2.

(Update 4/7/2023)

Researchers at the Chinese Center for Disease Control and Prevention (China CDC) have published an eagerly awaited analysis of swabs collected at a wet market in Wuhan, China, in the early weeks of the COVID-19 pandemic — as well as the underlying data, which the international research community has been calling for since the beginning of the outbreak.

The analysis, published in Nature on 5 April, confirms that swabs from the Huanan Seafood Wholesale Market — which closed in January 2020 and has long been linked to the start of the pandemic — contained genetic material from wild animals and tested positive for SARS-CoV-2. This suggests that it’s possible an animal could have been an intermediate host of a virus that spilled over to infect humans. But researchers say the latest findings still fall short of providing definitive proof that SARS-CoV-2 originated from an animal-to-human spillover event. (The study authors, led by former China CDC director George Gao, did not respond to requests for comment from Nature’s news team, which is editorially independent of Nature’s journal team.)COVID-origins report sparks debate over major genome hub GISAID

Still, researchers say that the publication of the genomic data, which have been deposited on open repositories, is crucial — because it will allow further analyses that could offer clues about the pandemic’s origin. “It’s one of the most important data sets we’ve had since the emergence of the pandemic,” says Florence Débarre, an evolutionary biologist at the French national research agency CNRS in Paris, who was part of a team that caused controversy by publishing its own analysis of the China CDC data last month. “They exist because at the time the right things were done.”

Evolutionary virologist Jesse Bloom says that although the swabs, which were collected in January 2020, provide useful information about what animals were at the market, even earlier samples are needed to find the pandemic’s origins. “If we ever learn the exact origins of SARS-CoV-2, I suspect it will come from new information about cases or events in early December or November of 2019, or earlier,” says Bloom, who is at the Fred Hutchinson Cancer Center in Seattle, Washington.

The paper is the latest in a series of published analyses of these market samples, and the first to be peer reviewed. The findings agree with a separate preprint analysis that the swabs contain genetic data from wild animals and from SARS-CoV-2. But these environmental samples do not confirm that any of the animals present were infected with the virus.

The Chinese team behind the latest report had published a preprint version of its study in February 2022 that did not include an analysis of animal genetic material in the swabs, and did not make public the underlying sequence data. The team that included Débarre found the China CDC swab data in the online genomics database GISAID and published its own analysis on the research repository Zenodo. That report identified wild-animal material in the swabs that tested positive for SARS-CoV-2 and pointed to animals, including raccoon dogs, as species of interest.

Contentious study

The latest report lends weight to one of the two competing theories about how the COVID-19 pandemic began. Debate has raged over whether it had a natural origin, with a virus passing from animals to humans, or arose from a laboratory leak at the Wuhan Institute of Virology.

The Huanan market has been at the centre of the natural-origin theory because several of the earliest known cases of COVID-19 were linked to the market. Animals that were sold there are known to be hosts for respiratory viruses called sarbecoviruses, which include SARS-CoV-2. However, the lab-leak hypothesis gained momentum in 2021 and has not been definitively ruled out.

A raccoon dog seen behind the bars of a cage
Genetic material from raccoon dogs was present in samples that tested positive for SARS-CoV-2 that were taken from the Huanan market.Credit: Viktor Kitaykin/Getty

The latest paper, like the Zenodo report, contains details about mammalian genomic sequences present in the market samples. The authors analysed 60 samples that tested positive for SARS-CoV-2 — 11 more than in the Zenodo report — and a further 112 swabs that were negative.

The findings support the natural-origin hypothesis, says a researcher who was not involved in either study and wishes to remain anonymous owing to the controversy surrounding COVID-origins work. The presence of many wild-animal species means that a viral spillover that resulted in the COVID-19 pandemic could have occurred, says the scientist. Some of those species, such as raccoon dogs, have the potential to transmit SARS-CoV-2 infections, the source adds. “The extent of circumstantial evidence [in the latest paper] is greater than one can find for the alternate hypothesis, which is that it leaked from a laboratory.”COVID-origins study links raccoon dogs to Wuhan market: what scientists think

The study also offers clues about the role of the market in the pandemic’s origin. In the early weeks of the outbreak, two lineages of SARS-CoV-2 — dubbed A and B — were circulating. Initially, tests identified only lineage B at the market. This led some researchers to conclude that the market might have acted only as a site for an early ‘superspreader’ event, rather than as a site of an animal spillover, because lineage A is thought to be more ancestral.

But the China CDC’s preprint posted last year identified lineage A in one sample. “It’s the result that really made me shift, that made me really say, ‘OK, it’s very likely to come from the market,’” says Débarre. But she says that some questioned whether the result was real. The new analysis confirms the presence of lineage A, addressing those doubts, she says.

David Relman, a microbiologist at Stanford University in California, agrees with the authors’ assessment in the study that the market might have acted as an amplifier of SARS-CoV-2 transmission. “It’s just as possible that humans brought the virus into the market, as animals might have.”

Spurious findings

Alice Hughes, a conservation biologist at the University of Hong Kong, has concerns about the quality of the analysis. As well as genomic fragments from animals including raccoon dogs, Hughes says that the paper identifies genetic material from pandas, mole rats and chimpanzees. Given that killing a panda attracts the death sentence in China, “there is absolutely no way any trace of panda could possibly be in that market”, she says.

The strange results could be from laboratory contamination, or improper processing of the data that failed to weed out spurious species identifications, says Hughes. “We must be exceedingly careful with interpreting or putting too much faith in the paper.”

Débarre also questions aspects of the results. The China CDC authors used two genomic-analysis methods: one that searches through all available genes and genomes, and another that zeroes in on specific sequences in the mitochondrial genome. The whole-genome method detected only a few raccoon-dog sequences in a sample that was full of raccoon-dog nucleic acids, according to the Zenodo analysis and the China CDC’s mitochondrial genome analysis, says Débarre.

The data do not clearly point to a specific animal as an intermediate host that passed the virus onto humans. But the researcher who wished to remain anonymous says that the results again highlight some animals, including raccoon dogs, that can be studied for how well they transmit SARS-CoV-2.

Débarre says that further forensic analyses could reveal whether any animal DNA in the swabs bears signs of immune-system activation, which could indicate active infection. That could help to address concerns that the presence of virus and animal DNA in the same sample does not necessarily indicate that an animal was infected.

But Relman doesn’t think that further analyses of the same data set could lead to significant answers about the virus’s origin. “What we really need are other kinds of data. Good verifiable data on the early clinical events in Wuhan.”

For some long COVID patients, exercise is bad medicine

​They used to run marathons. Now, taking a shower is exhausting. But for these patients—who have one of the most debilitating symptoms of long COVID—hope may be on the horizon.

(Update 4/28/2023)

When Jessica Lambert was seen at a Chicago long COVID clinic in May 2021 after months of debilitating symptoms, a physical therapist told the formerly active, 37-year-old she was out of shape and started her on an exercise program. Lambert left the sessions exhausted, a fatigue beyond anything she’d ever felt after weightlifting and cycling. The next day she would wake up feeling worse. Forty-eight hours after therapy, her symptoms peaked, with a fever, deep muscle pain, nausea, and a migraine.

“I couldn’t get out of bed, except to move to the couch,” she says. “I’d stay there for the next four or five or six days and start climbing out of it just in time for my next appointment.” After two and a half months of weekly physical therapy sessions and a trip to visit her mother, she spent four months bedridden. Eventually, following a second bout of COVID, she could no longer walk at all.

Lambert didn’t know it, but she was experiencing post-exertional malaise, or PEM, one of the most mysterious and debilitating symptoms of long COVID. Defined as the significant worsening of symptoms or the development of new ones following even minor physical, mental, or emotional exertion, a PEM “crash” can take days, weeks, or months to recover from, and some people claim they never do. Almost 80 percent of an estimated 16 million adult long COVID patients in the U.S. say they are limited in their day-to-day function, a quarter of them significantly. About half have had to reduce work hours, and as many as four million long COVID patients in the U.S. are out of work altogether.

“People come in and tell me, I used to work out. I used to run. I used to love my job as the vice president of my company. And now I can’t do any of that,” says Mark VanNess, a researcher with the Workwell Foundation, which studies PEM in long COVID and other related chronic illnesses. “These are not people that want to stay home and collect disability. They’re forced to.”

In one study, about 75 percent of the almost 500 long COVID patients surveyed said physical activity made their symptoms worse, while less than one percent saw improvement. Still, in long COVID patients like Lambert, PEM is often ascribed to deconditioning—the effects of being inactive—that can be treated with exercise. But the narrative of deconditioning is slowly starting to change. “You used to run marathons and after a three-week viral infection you’re somehow unable to walk across one side of your apartment to the other? That’s not deconditioning,” says David Putrino, the director of rehabilitation innovation for the Mount Sinai health system in New York.

As doctors struggle to treat the approximately 65 million people worldwide with long COVID, PEM has ignited a debate about the role of physical activity in rehabilitation: Exercise is generally considered a universal medicine, but can it make some long COVID patients worse?

What is PEM?

For decades, PEM has been a hallmark symptom of myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS), a little-understood illness usually manifesting after a viral infection. About half of long COVID patients meet the criteria for ME/CFS. “When we started seeing long COVID, we thought, This looks pretty darn familiar,” says Brayden Yellman, a physician who treats ME/CFS and long COVID patients at the Bateman Horne Center in Utah. People with ME/CFS rate lower on quality-of-life measures than those with cancer, stroke, and multiple sclerosis—in large part because of PEM.

How PEM presents varies widely. A shower can leave some confined to bed for days. A short visit with friends can cause flu-like symptoms and trouble speaking. Watching a movie can lead to migraines and light sensitivity. Most of the afflicted describe a profound fatigue that can feel like a conscious coma, where they are unable to move or talk. “I’ve had patients say to me, If the house was on fire, I’m not sure I’d be able to get out,” Yellman says.

Because the onset of PEM is often delayed by 24 to 72 hours after exertion, patients may appear functional one day, then crash the next, making it hard to track. And, since there is no official diagnostic code for PEM, its prevalence in long COVID patients is difficult to determine via electronic health records, where it can appear as exercise intolerance or fatigue, two related but different symptoms. Patient surveys suggest that the percentage of COVID long haulers experiencing some form of PEM may be more than 90 percent.

In ME/CFS, PEM has historically been dismissed or downplayed as a combination of deconditioning and a psychological fear of exercise. Physicians prescribed graded exercise—therapy in which the intensity of physical activity is increased incrementally—and while some studies show it had a positive effect, between half and three-quarters of patients reported it made them worse. Eventually, many of the studies were criticized or independently discredited, and both the U.S. and U.K. governments removed graded exercise from ME/CFS official treatment guidelines. Still, exercise is commonly prescribed to long COVID patients: half of the current 388 international long COVID clinical trials are focused on rehabilitation, many involving exercise.

Biological causes of PEM

A growing trove of research shows that PEM has physiological underpinnings. In cardiopulmonary exercise tests spaced 24 hours apart designed to trigger PEM, researchers find that while active people, sedentary people, and even people with conditions like heart disease and cystic fibrosis perform generally the same from one day to the next, people with ME/CFS do worse on the second test. Other studies find that ME/CFS patients show decline on cognitive tests post-exercise while healthy people perform better. The studies also show these patients are missing certain metabolites in their urine, which suggests their bodies aren’t performing the necessary functions to recover.

Research by David Systrom, a physician at Brigham and Women’s hospital in Boston, might provide a hint as to why. When ME/CFS patients and those with long COVID exercise, Systrom discovered their veins were not moving blood to the heart efficiently, or “priming the pump.” He also found problems with oxygen exchange by the exercising muscle. Through skin biopsies, he sees nerve damage in most patients he tests. “It’s not what we’d expect in pure deconditioning,” Systrom says.

Systrom’s work points to a dysfunctional autonomic nervous system, which controls functions like breathing and circulation, and moves blood and oxygen through the body during and after exercise. He also theorizes that the mitochondria—the parts of our cells that make energy—might not harness oxygen correctly. This all impairs the body’s ability to recover.

Does exercise lead to decline?

The concept of long-term decline after pushing through exertion is well-known amongst providers who treat ME/CFS, and now long COVID.

“Repeated crashes of PEM are like an injury,” Yellman says. “If you stub your toe really hard on the door, you need to let it heal before you put your shoe back on. If you stub it every day, there’s going to be scarring and the toenail isn’t going to grow back.”

The answer, according to physicians familiar with PEM, is pacing—managing daily activities through periods of exertion and rest. It’s critical, Yellman says, to break what he calls “the push-crash cycle,” by learning to recognize energy limits and resting accordingly, which for some people can take months or even years. “I’ve never met a couch potato with this illness,” he says. “A type A personality is honestly a risk factor.”

Clayton Powers, a physical therapist with the University of Utah, first learned about PEM five years ago, while treating patients with postural orthostatic tachycardia syndrome (POTS), a type of autonomic nervous system dysfunction also common in long COVID that can be helped by a form of graded exercise. But he noticed many of his patients weren’t improving with his exercise prescriptions.

He changed his tactics, focusing instead on using heart rate monitors, education, and lifestyle modifications to help patients avoid PEM. “The amount of improvement switching from exercise to focusing more on pacing and energy conservation was drastic,” he says.

With a growing awareness of cases like Lambert’s, patients, advocacy organizations, clinicians, and researchers are pushing back against the National Institutes of Health’s $1.15 billion RECOVER project’s proposed exercise trial for long COVID. Duke University’s Clinical Research Institute, which is coordinating the study, says it’s aimed at combating exercise intolerance, fatigue, and other long COVID symptoms. In an emailed statement, the institute noted that “exercise is not recommended” for those experiencing PEM and claims researchers will carefully monitor for PEM and adapt the program accordingly, but does not explicitly say whether participants with PEM would be excluded.

Even if the trial successfully screens for PEM, advocates suggest that government funds for the five planned clinical trials might be better spent on testing pharmacological treatments that could help more long COVID patients and others with post-viral illness.

Is all exercise equal?

With long COVID encompassing about 200 symptoms, some patients may benefit from exercise. But doctors must know how to carefully screen patients before prescribing an exercise regimen. It’s part of why advocates are now petitioning the Centers for Disease Control and Prevention to create an official diagnostic code for PEM, hoping it will drive recognition, provide a way to track it, and give patients and providers clear guidance on treatments.

The U.S. ME/CFS clinician coalition is against exercise, Yellman says. “But the real answer is, it’s still good for you, if you can avoid PEM.” Yellman, Systrom, and other physicians who treat ME/CFS and long COVID emphasize that they don’t recommend any exercise until, after a combination of medication, treating comorbidities, and pacing, a patient can consistently perform daily activities without triggering PEM. Even then, what they prescribe is far less strenuous than what most people consider traditional exercise.

“If exercise is medicine, you should treat it like medicine,” Putrino says. “You should understand what the contraindications are, who might have adverse effects of the medicine, and how to dose the medicine effectively for each person.”

Putrino and his colleagues developed a specialized rehabilitation program to help some long COVID patients reboot their autonomic nervous systems. In it, patients slowly progress through a series of gentle movements while lying down and doing breathing exercises that promote their “rest and digest” response. Then they move to sitting and upright exercises over the course of a few months. But, unlike graded exercise that encourages patients to push through discomfort, the program is scaled back to about 30 percent of the previous effort at the first sign of PEM, and some people won’t progress past a certain level. Still, according to Putrino, after three months, most participants see fatigue halve and activity tolerance double.

The therapists in Jessica Lambert’s in-patient rehabilitation program employed a similar strategy to help her regain her ability to walk.

“They would start off with me laying down in bed, lifting one leg at a time, then resting,” she says. She eventually progressed to seated activities, like wheelchair yoga, that focused on her ability to better care for herself. Now she’s in physical therapy doing recumbent exercises, and the therapists pull back if she experiences PEM. In a year, she’s gone from being in a wheelchair to being able to walk slowly around the block. “It’s small,” she says, “but it feels huge.”

COVID’s future: mini-waves rather than seasonal surges

Three years after the start of the pandemic, SARS-CoV-2 shows no signs of settling into a seasonal pattern of spread, like influenza has.

(Update 5/3/2022)

Whether you call it a surge, a spike, a wave or perhaps just a wavelet, there are signs of a rise in SARS-CoV-2 infections — again. A growing proportion of tests in some countries are coming back positive, and new variants, most notably a lineage called XBB.1.16, are pushing aside older strains, fuelling some of the uptick in cases.

Welcome to the new normal: the ‘wavelet’ era. Scientists say that explosive, hospital-filling COVID-19 waves are unlikely to return. Instead, countries are starting to see frequent, less deadly waves, characterized by relatively high levels of mostly mild infections and sparked by the relentless churn of new variants.Are repeat COVID infections dangerous? What the science says

Wavelets don’t always create a dramatic spike in hospitalizations and deaths; their effects on health vary between countries. But the relentless series of wavelets looks very different from the slower, annual circulation patterns of influenza and cold-causing coronaviruses, and it seems increasingly unlikely that SARS-CoV-2 will settle into a flu-like rhythm anytime soon, say scientists.

“We haven’t slowed down in the last year, and I don’t see what factors would cause it do so at this point,” says Trevor Bedford, an evolutionary biologist at the Fred Hutchinson Cancer Center in Seattle, Washington. “It will be a continually circulating respiratory disease. It may be less seasonal than things we’re used to.”

Victorious variant

In March, scientists in India started seeing signs that a new SARS-CoV-2 variant was causing a rise in infections. The XBB.1.16 lineage has displaced others that drove case surges in India several months ago, says Rajesh Karyakarte, a microbiologist at Byramjee Jeejeebhoy Government Medical College in Pune, India. “We see that it has almost replaced all other variants in India, and we think the same thing will be followed everywhere.”

In a study posted to the preprint server, Karyakarte and his colleagues analysed more than 300 cases, from last December to early this month, and found that XBB.1.16 infections tend to cause mild symptoms similar to those from earlier Omicron variants, with few hospitalizations and deaths. “We didn’t see much,” Karyakarte says. The study has not yet been peer reviewed.How your first brush with COVID warps your immunity

The World Health Organization declared XBB.1.16 a ‘variant of interest’ on 17 April. But whether it or another new variant will cause a spike in infections in a particular country will probably depend on the size and timing of the country’s earlier waves, says Tom Wenseleers, an evolutionary biologist at the Catholic University of Leuven in Belgium.

He estimates that XBB.1.16 is spreading fairly rapidly in the United States, where it is now estimated to make up more than 11% of cases. In Europe, the variant is less prevalent and is spreading more slowly. This could be due to Europe’s relatively large and recent spike in infections caused by a closely related variant, XBB.1.5, which struck earlier in the United States.

Wavelet, surge, repeat

Some countries are experiencing surges of infections three or four times each year, driven largely by the breakneck pace at which the virus continues to change, says Bedford. Currently, SARS-CoV-2’s spike protein, in which most immunity-evading mutations occur, is evolving at twice the rate of a similar protein in seasonal influenza and about ten times as quickly as those of cold-causing ‘seasonal’ coronaviruses.

Influenza and common-cold coronaviruses cause seasonal epidemics in part because of favourable transmission conditions, such as people spending more time indoors during winter. The combination of rapid mutation and short-lived human immunity is probably preventing SARS-CoV-2 from settling into seasonal patterns of circulation, says Wenseleers.

The stubbornly high frequency of SARS-CoV-2 surges translates to large numbers of infections. Data from the now-defunct UK survey of SARS-CoV-2 prevalence suggested that the country experienced as many infections as it has residents in the last year, which equates to a 100% annual ‘attack rate’, says Bedford. In the future, “we can still imagine 50% attack rates every year, half the population getting infected”, compared with around 20% with influenza.

Emulating influenza

There is little doubt, however, that SARS-CoV-2’s continuing ebb and flow is causing fewer problems than in the past.

In South Africa, the country’s health systems would quickly send notice if COVID-19 hospitalizations and deaths were on the rise, says Waasila Jassat, a public-health specialist at the country’s National Institute for Communicable Diseases in Johannesburg. “That doesn’t seem to be have been the case for many, many months,” she says.

In the year and half since Omicron emerged, COVID-19 deaths remain stubbornly high and the toll has been around ten times higher than that typically caused by influenza, says Wenseleers. But, still, large infection waves are causing smaller ripples in hospitalizations and deaths. “It gives most people the hope that, in the coming years, the net toll of COVID will get comparable to influenza,” he says.

WHO declares end to COVID-19’s emergency phase

The pandemic has been on a “downward trend”, but the risk of new variants remains, says WHO director-general.

(Update 5/10/2023)

The World Health Organization (WHO) announced on Friday that COVID-19 is no longer a public health emergency of international concern (PHEIC). The WHO director-general, Tedros Adhanom Ghebreyesus, made the decision following a recommendation by the organization’s COVID-19 emergency committee. During a meeting on Thursday, the committee highlighted the decreasing numbers of deaths and hospitalizations and the high levels of population immunity against SARS-CoV-2 as reasons for ending the PHEIC.

During a press conference the next day, Tedros emphasized that COVID-19 remains a global health threat and that the new status doesn’t mean that countries can let down their guard. “It is time for countries to transition from emergency mode to managing COVID-19 alongside other infectious diseases,” he said.

The announcement didn’t come as a surprise. After the emergency committee’s last meeting, in late January, Tedros acknowledged that the pandemic was probably at a transition point.

“This is not a snap decision. It is a decision that has been considered carefully for some time, planned for, and made on the basis of a careful analysis of the data,” he said during the press conference.

Practical impacts

A PHEIC — defined by the WHO as an extraordinary event that constitutes a public-health risk to other countries through the international spread of disease — is the highest level of international public-health alarm. The COVID-19 PHEIC was declared on 30 January 2020. In practice, this decision compelled countries to start reporting cases to the WHO to create worldwide surveillance. “Importantly, [a PHEIC is] signalling to all countries that they need to prepare,” says epidemiologist Salim Abdool Karim, the director of the Centre for the AIDS Programme of Research in South Africa, in Durban.

In the three years, three months and five days that have passed since the COVID-19 PHEIC was established, countries have reported almost seven million deaths to the WHO. But the pandemic’s true death toll could be two to three times higher, according to estimates from the WHO and others.

There are no hard and fast rules to determine when a PHEIC is over, says Karim. “We are still very much in a pandemic, we are just in a different stage in which we are no longer seeing large numbers of deaths and pressure on hospitals,” he adds. For Karim, the end of the PHEIC is a recognition that SARS-CoV-2 is no longer an emergency, but it will be around for a long time.

Although he says the decision was pragmatic and reasonable, he worries about the effects on resources and the availability of diagnostic tests, vaccinations and treatments.

Epidemiologist Jennifer Nuzzo, the director of the Pandemic Center at Brown University, in Providence, Rhode Island, says it is unclear whether this decision will have much of an impact, given that many countries have already been relaxing measures to combat COVID-19. “Political attention to the pandemic was lost long before this decision, unfortunately,” Nuzzo says. “Even while COVID remains a top cause of death, governments have decided to put their energies elsewhere.”

Nuzzo says it’s important to distinguish between the end of the PHEIC and the decision by individual countries to end their public-health emergencies. The United States, for example, has announced that its COVID-19 health emergency will end on 11 May. That means that some disease monitoring and surveillance will cease and some US residents could lose access to free COVID-19 testing, vaccines and treatment. “It will worsen the inequity in the access to diagnostics and treatments, and that’s my concern,” Karim says.

The path forward

In his statement, Tedros said he has decided to establish a review committee to develop long-term recommendations for countries on how to manage COVID-19. On Wednesday, the WHO published an updated version of their strategic preparedness and response plan for COVID-19, outlining actions that countries should take in the next two years.

“What is most urgent now is to make sure that countries don’t turn their back on trying to learn the lessons of COVID and bolster their preparedness for future pandemics,” Nuzzo says.

Why is COVID life-threatening for some people? Genetics study offers clues

Immune genes could play a part in the risk of needing intensive care when infected with SARS-CoV-2.

(Update 5/19/2023)

An analysis of DNA from more than 24,000 people who had COVID-19 and required treatment in intensive care has yielded more than a dozen new genetic links to the risk of developing extreme illness from the disease.

The study, which was published on 17 May in Nature and has more than 2,000 authors, highlights the role of the immune system in fuelling the later stages of particularly severe COVID-19. The results could one day contribute to the development of therapies for COVID-19 — and potentially other diseases that cause acute respiratory distress or sepsis.

“These are likely to be processes that are active in other conditions,” says Kenneth Baillie, an intensive-care specialist at the University of Edinburgh, UK, and lead author on the study. “Everything that we’ve done in COVID will, I think, be relevant to other groups of patients that we haven’t identified yet.”

Team effort

Much of the data were collected from people who were infected with SARS-CoV-2 during the first waves of the pandemic in the United Kingdom. At that time, many intensive-care staff members were terrified of spending time on the ward, says Baillie. A coronavirus outbreak in 2003 caused by the related virus SARS-CoV had a mortality rate of about 10% and had hit health-care workers particularly hard. “We were nervous,” says Baillie. “Certainly, in the first wave of the pandemic, and for some people in subsequent waves, it seemed like a considerable personal risk.”

Despite their fear and the frenzy of providing care at the onset of the pandemic, scores of health-care workers took on the added burden of enrolling participants in studies that investigate how genetics might have contributed to disease severity. Many of the participants were on ventilators, and enrolling them meant long discussions with relatives who were going through some of the most difficult times of their lives, says Baillie. The result was an effort called GenOMICC, which researchers hope will help to improve treatment options for COVID-19 and other conditions in future pandemics.How your first brush with COVID warps your immunity

Baillie and his colleagues analysed data from more than 24,000 people and combined this information with data sets from around the world. They found 49 DNA sequences that are associated with becoming critically ill from COVID-19. Sixteen of these had not been reported previously.

Among these sequences are some that could affect the activity of genes and proteins involved in the immune system. Raging immune cells have long been implicated in causing some of the tissue damage seen in late-stage, severe cases of COVID-19. Baillie and his colleagues found genetic links to inflammatory responses and the activation of immune cells — processes that can damage the lungs and reduce their capacity to send oxygen to the body’s tissues.

“It definitely expands our understanding of the genetic determinants of severe COVID,” says Brent Richards, a human geneticist at McGill University in Montreal, Canada. Richards is an investigator on another project called the COVID-19 Host Genetics Initiative, a global effort in which scientists from more than 54 countries share data.

The diversity of that effort will provide a crucial counterpart to the GenOMICC study, which is predominantly drawn from participants of European descent, says Richards.

Reliable results

In addition to the new findings, it is important that the UK study has replicated many of the findings by other groups, says Alexander Hoischen, a geneticist at Radboud University Medical Center in Nijmegen, the Netherlands. Replication of results across different data sets is crucial when trying to tease apart the possible contribution of common genetic variants to disease.

Even so, it will take a great deal of work to show that these variants contribute directly to critical illness — a necessary step to turn these initial findings into new therapies. “That is still a long trajectory,” says Hoischen.

But putting together these large consortia of investigators and taking the first steps are considerable triumphs, he adds. In the early days of the pandemic, it was unclear how participation in such large endeavours would benefit the careers of individual scientists. “Many of them acted as purely human beings,” he says, instead of worrying about their careers. “It illustrates the degree of solidarity that we really witnessed in COVID times.”

How COVID-19 harms the heart

Many patients are experiencing heart palpitations, chest pain, and shortness of breath even after recovering from COVID-19. But new studies offer reason for hope.

(Update 8/11/2023)

Danielle Huff was on her treadmill when she first noticed the pain in her chest. She had just recovered from a terrible case of COVID-19 about two or three weeks earlier, during which she’d had just about every symptom imaginable: sore throat, headache, congestion, coughing, loss of smell, body aches, a mild case of pinkeye, and a constant heaviness in her chest like there was a bowling ball weighing it down.

But this feeling in her chest was different—it was a sharper pain that came on suddenly. Huff, an Illinois school administrator in her 30s, has a family history of heart issues, and she worried that it might signal something serious. Although she’d always tried to live a healthy lifestyle—doing yoga or walking every day—she soon found herself too frightened to exercise.

“It got to the point where I just couldn’t,” she says. “I was scared of the chest pain because I didn’t know what it was.” Ultimately, her doctor referred her to a cardiologist who specializes in treating patients who have recovered from COVID-19 but still experience cardiac symptoms.

From the earliest months of the pandemic, scientists have suspected that COVID-19 is not just a disease of the lungs, but also a disease of the heart and blood vessels. “We realized very, very early that clotting was playing a major role,” says Jeffrey Berger, director of New York University Langone’s Center for the Prevention of Cardiovascular Disease. Even in March 2020, physicians were seeing unexpectedly high rates of blood clots in their patients, leading to a rise in heart attacks and strokes. Autopsies also revealed masses of tiny blood clots in places where doctors don’t normally see them, such as the liver and the kidneys.

Now it has become clear that COVID-19’s cardiovascular damage doesn’t resolve as soon as a patient recovers from the initial infection. For some patients, MRI scans show signs of inflammation months after clearing the virus. Others continue to have elevated levels of troponin, a chemical that’s released into the blood whenever there’s damage to the heart muscle.

Oddly, Huff took a battery of heart-related tests and the results came back normal. Still, she found herself so short of breath she had to step out of a yoga class and couldn’t walk across her school building without needing to sit down. And about a month after she recovered from COVID-19, she began feeling random heart palpitations.

Adding to the mystery, some people who had only mild or even asymptomatic cases of COVID-19 also report long-lasting symptoms such as heart palpitations, chest pain, shortness of breath, and extreme fatigue. Scientists are still baffled about what’s causing them.

“To me there’s no question these individuals are suffering real symptoms,” says James de Lemos, a cardiologist at the University of Texas Southwestern Medical Center and a co-chair of the American Heart Association’s COVID-19 CVD registry steering committee. “The question is, is there some injury to the heart that’s leading to symptoms that we’re not seeing?”

There is reason for hope. Researchers have made strides toward understanding how to prevent COVID-19 from attacking the heart and blood vessels. Meanwhile, physicians are learning more every day about how to treat long COVID symptoms—and rigorous investigations are underway to help shed light on why they occur.

How COVID-19 attacks the cardiovascular system

Physicians quickly learned in early 2020 that the use of blood thinners, which help keep blood from clotting, improved the chances of survival for moderately ill COVID-19 patients. But Berger says it also became clear that there was more to the deadly blood clotting than what they could treat with these anticoagulant therapies alone.

“One in four patients were still dying or requiring organ support,” he says.

In the last five to 10 years, scientists have begun to understand that platelets play a role in promoting unwanted clotting and inflammation in other diseases such as HIV, psoriasis, lupus, and rheumatoid arthritis. These tiny round blood cells serve one major purpose: to stop bleeding by binding to a damaged blood vessel and forming a clot. With that in mind, Berger and a team of researchers set out to investigate what role the platelets might play in COVID-19.

“We found it was nothing like we would have expected,” Berger says. “It was like somebody changed the genetic architecture of these platelets.”

In a study published in Science Advances, the researchers showed that the virus can enter megakaryocytes, the bone marrow cells that make platelets. The infected cell then alters the genetic material in the platelets so that they become more active and give off protein signals that make the lining of the blood vessels sticky and inflamed. This makes the vessels prone to developing clots that can spread throughout the body.

Scientists also learned that the virus weakens connections in the tissue that lines blood vessels, making them leaky instead of sealing them up, as you might expect when clots are present.

“It’s like a double-edged sword,” says Ben Maoz, a biomedical engineer at Tel Aviv University and lead author of a recent study that identified the SARS-CoV-2 proteins that cause the most damage to the blood vessel lining. Somehow, he says, COVID-19 affects the blood vessels “in a dual and opposite way.”

Leaky vessels allow blood and other chemicals in the body to spill into places they’re not supposed to go—including the air sacs of the lungs and the tissues of other organs. That can have a cascade of downstream effects, from the flooded lungs seen in many severe COVID-19 cases to complications of the liver, kidneys, and, of course, the heart.

“Things we’re supposed to be protected from are suddenly coming in,” Maoz says. He likens the harm this causes to a garbage bag with holes in it: Those holes will allow some waste to seep back into your home. Some of the subsequent damage, like the smell and the foul liquid, will be noticeable right away. But others—like, say, a resulting rat infestation—may not be evident for months. The extent of that harm will depend on how bad the leak was and how long it lasted.

Post-COVID symptoms

But it’s not clear exactly how this blood vessel damage is connected to the lingering cardiovascular symptoms in patients who have recovered from COVID-19. Maoz points out that the virus causes harm in many complex ways that are difficult to disentangle. Yet physicians have continued to see signs of damaged heart tissue such as myocarditis, inflammation of the heart muscle, or high levels of troponin months after hospitalization from COVID-19.

Berger says it’s not unusual for a virus that causes such severe inflammation to have residual consequences post-recovery—particularly among patients who had moderate or severe disease and needed to be hospitalized. Worryingly, some patients who had asymptomatic, mild, or moderate disease—including children—also have similar evidence of heart damage. (The real risk of heart inflammation to kids is from COVID-19—not the vaccine.)

Yet mounting evidence suggests that myocarditis due to COVID-19 is more rare than initially believed, de Lemos says. In September a Centers for Disease Control and Prevention study showed that the risk of myocarditis is nearly 16 times higher in patients with COVID-19 than those without. However, the study concluded that the condition is uncommon for both populations—and the risk of myocarditis from COVID-19 is just 0.146 percent. De Lemos says the condition also does heal within months.“

Most of those hearts look fairly normal when reevaluated during follow-up,” he says.

Then there are patients like Huff. Amanda Verma, a cardiologist who treated Huff at the Washington University School of Medicine’s post-COVID clinic in St. Louis, says that some patients come in with chest pain but their stress tests are normal. Others complain of palpitations, yet when equipped with heart rate monitors, their heart rhythms appear normal. Still, Verma says those tests aren’t telling the whole story.

“If you dig a little deeper, you’ll notice that the heart rate pattern isn’t quite normal,” she says. Although it’s expected for a person’s heart rate to rise while walking, it’s not normal for the heart rates of younger and athletic patients to jump from 60 to 120 just from walking across a room or while they’re asleep—which is what was happening to Huff.

This abnormal increase suggests COVID-19 triggered dysfunction in the autonomic nervous system, the pathways of nerve cells that automatically control vital functions such as breathing and the heartbeat, Verma says. It’s part of the evolutionary “fight or flight” response that allows your body to function without having to be consciously instructed. For COVID-19 long-haulers, that system appears to be out of whack.

“People often tell me they’re exhausted by the end of the day—and, yeah, who wouldn’t be if your heart rate was up that high all day?” Verma says. “It’s like you’ve been running all day.”

Scientists have yet to understand how COVID-19 might be causing this type of dysfunction. Some hypotheses suggest it could be a result of the body’s excessive inflammatory response to the virus, or perhaps it could even be related to sex hormones, since women are more likely than men to become COVID-19 long-haulers. Either way, the inability to name the syndrome makes it challenging to get insurance companies to cover treatments—and is maddening for patients who feel their symptoms are not being taken seriously.

“It’s unbelievably frustrating for patients who suffer from this because they don’t get answers,” de Lemos says. “To some extent validating that this is real is the first step. This is real illness, and we just don’t understand it yet.”

Reasons for hope

Researchers are making progress on finding treatments that could reduce the severity of COVID-19—and ultimately improve cardiovascular outcomes. Berger and his team are studying drugs that target the platelets to prevent them from activating and causing clotting.

Meanwhile, Maoz and his team have identified the five virus proteins that cause the most harm to the blood vessel lining. They are testing a model that will allow researchers to identity the proteins that inflict damage on other parts of the body. This molecular understanding will help to develop drugs that can block the specific proteins from attacking the blood vessels and causing critical illness.

“It’s amazing to see how fast we’ve been able to adapt and answer fundamental questions,” Berger says. “The speed of science has dramatically improved.”

However, he acknowledges that none of these potential drugs that would prevent the platelets from clotting or block the virus proteins from attacking the blood vessels will help people who are already suffering from long COVID. To do that, scientists ultimately need to figure out what’s behind their strange constellation of symptoms.

Earlier this year, the National Institutes of Health launched a collaborative research initiative that will support large-scale studies of long COVID-19 in children and adults. And Verma says that physicians who specialize in long COVID-19 are starting to find ways to treat it, from prescribing anti-inflammatories for chest pain to beta blockers for reducing a patient’s blood pressure when their heart rate is out of control. Even exercise—when carefully monitored and structured so that it doesn’t exacerbate fatigue—can help.

There’s also anecdotal evidence that long COVID can resolve over time—even if that may take a year to 18 months. Verma says she’s been able to take some of her patients off their medication, and many of those who haven’t recovered completely do eventually feel better after treatment.

“The big question though is, is this going to impact their health in 10 or 15 years down the road?” she says. “Did it do something we just can’t see?”

For Huff, things have gotten better. After taking medications for her high blood pressure and elevated heart rate, the palpitations and shortness of breath have dissipated. Intriguingly enough, so did the frequent migraines that she’s had since she was 13. She’s still too afraid of the chest pain to go back to exercising, but she’s hopeful for the answers that ongoing research and open communication between doctors and their patients may yield as they learn together about the long-term implications of COVID-19.

“There’s a lot to learn, and I can understand the frustration with not knowing what’s going on,” she says. “But I’m at a point of acceptance that I’m just not going to have all the answers right now.”

COVID cases are rising again. Here’s a refresher on everything you forgot.

Can you use an expired test? How long do you need to isolate? With more infectious variants, here’s a reminder on how to protect yourself—and what to do if you get sick.

(Update: 9/20/2023)

A new posse of infectious Omicron variants are causing more people to come down with COVID-19, and some are getting extremely sick. In the last week of August more than 650 people died from the disease—up 10 percent from the prior week—and 17,000 new patients were hospitalized.

With updated vaccines recently approved by the U.S. Food and Drug Administration, the U.S. Centers for Disease Control and Prevention recommended the shots for all Americans older than six months. Experts hope the immunity most Americans gained from prior bouts of COVID, past shots, and/or the vaccine that will be available within days, will make surges like one in early 2021—when some 20,000 people died each week due to COVID-related complications—less likely.

It’s unclear whether this late summer bump might indicate an annual pattern, since COVID-19 is too new to have seasons like the flu does, says Rick Martinello, an infectious disease expert at the Yale School of Medicine in New Haven, Connecticut. One factor contributing to the recent uptick in cases are the heat waves that baked much of the country last month, forcing people indoors where viruses spread more easily.

“Whether we’ll see cases rise a bit and plateau soon or instead have a significant peak is something we just don’t know right now,” Martinello says.

With the number of cases on the upswing, here are some reminders and recommendations about how to protect yourself and what to do if you think you have the virus or get sick.

Have your old COVID antigen tests expired? 

The COVID antigen tests you bought in the pharmacy or received free from the federal government are stamped with an expiration date, after which you are supposed to discard them. Many manufacturers received approval to extend their expiration dates after the tests were distributed.

But those past the extended expiry dates may still perform sufficiently, says Zishan Siddiqui, an assistant professor of medicine at the Johns Hopkins School of Medicine in Baltimore. He and his colleagues placed small viral samples on two groups of Abbott’s BinaxNow tests—some within the extended expiration date and others five months past—and found both performed similarly. (One difference: the positive line on expired tests was often fainter, indicating that older tests should be evaluated in bright light.)

“I think it’s reasonable for people to use an expired test they have at home,” Siddiqui says, especially if the alternative is not testing at all. Still, older kits, especially those stored in hot locations or crammed together, may have damaged swabs or test cards or degradation of important testing chemicals.

Anyone who has respiratory symptoms and gets a negative home test (whether expired or not) should follow guidance from the CDC and take another test two days later.

Swab the throat or the nose?

It turns out nasal samples concentrate more of the virus and are therefore more likely to yield a positive diagnosis. Plus, antigen tests were not designed for oral samples that could contain bacteria or other contaminants, Siddiqui says.

Can you get sick within days of SARS-CoV-2 exposure?

A recent study in France confirmed what people are feeling, that those exposed to Omicron develop symptoms earlier than they did after exposure to the original SARS-CoV-2 strain.

It’s possible that the incubation period is shorter due to the mutations. But it’s also likely these changes reflect improved understanding of when the virus is contagious, Martinello suggests.

Even today people vary greatly in how quickly they get sick. “I don’t think we yet fully understand what the incubation period for COVID is,” Martinello says.

How long should you isolate if testing positive for COVID?

Whether a person has a positive test or is likely to have the disease based on symptoms and exposure, it’s crucial they go home and immediately isolate from everyone, including people with whom they live.

This isolation should continue for a minimum of five days, which starts the day after the positive test or the appearance of symptoms, according to the CDC.

A sick person who shares a home should remain in a separate room and wear a mask during any brief forays to the bathroom or kitchen, Martinello says. (Fellow residents should wear a mask when they enter a shared space.) Weather permitting, they might open a window to disperse the virus. If they own a HEPA air filter it should be placed in the room near the head of the sick person’s bed, a location that captures more virus particles than outside the door or in other parts of the home.

The isolation period can end after five days if symptoms never developed, or after the person is improving and is free of fever (without drugs) at least 24 hours. Those with serious symptoms like shortness of breath or who have been hospitalized should isolate at least 10 days.

When is masking after isolation necessary? 

Once in public, the individual must wear a high-quality mask until 10 days have passed since symptoms began or testing positive. Remember: the first day is day zero. This is important because the sick person could be contagious for a full 10 days.

Researchers found that half of the National Basketball Association players repeatedly tested in 2021 still had high viral levels on day five. (If feasible, it is preferable to remain isolated at home longer than five days, Martinello says.)

However, it is safe to unmask before day 10 if two home antigen tests taken two days apart both yield negative results.

Who should take the antiviral drug Paxlovid? 

Those who are most likely to face hospitalization and death should talk with their healthcare provider about taking the antiviral medicine, Paxlovid, which continues to be effective against current strains. Vulnerable groups include people older than 50, those of any age who have not been vaccinated, and people 12 or older with serious medical conditions—chronic lung, liver, heart or kidney disease, cancer, diabetes—and those who are immunocompromised or have a weakened immune system (including from medications). 

This should be done early, as the medicine works only when started within five days after symptoms begin. Another option for people at high risk who can’t take Paxlovid is a three-day IV infusion of Remdesivir, which similarly blocks replication of the virus.

Some worry about getting a rebound case of COVID following Paxlovid, but it’s unclear whether the rebound is caused by the drug or by the disease. (Read more about why COVID rebounds aren’t definitively linked to Paxlovid.)

Should you get the new vaccine? 

The FDA and CDC recently approved new COVID vaccines for people six months and older. The benefits of vaccination outweigh side-effect risks for all these age groups, the CDC noted.

These mRNA shots from Moderna and Pfizer no longer target the original strain of SARS-CoV-2 but instead aim for the Omicron variant XBB.1.5 that more closely mirrors the strains currently circulating. Only a single dose is required, even for people who have not gotten prior vaccinations. (Children under five may require multiple doses.)

“Staying up to date on vaccines is the most effective tool in your toolkit,” says Vandana Madhavan, an infectious disease expert at Massachusetts General Hospital’s pediatric hospital in Boston.

In addition to preventing serious illness, vaccinations seem also to reduce the risk of developing long COVID following an infection.

How else can you protect yourself?

Avoiding crowds and masking remain extremely effective protection measures, but most people don’t need to do them 24/7. “Prevention is not an on-off switch but is more like a dimmer that you turn up or down depending on what is happening in the community or in your life,” Madhavan says.

People who have risk factors for severe disease or who live with people who do may need to keep the switch on brighter more of the time. But others might stay home more or wear face protection in crowded situations like public transportation, supermarkets, or the movies primarily when local caseloads are high or when they really want to avoid getting sick, perhaps because of an upcoming family wedding or vacation, she says.

Even when only one person wears a mask they are protected. Research by the CDC makes clear that someone who wears a high-quality mask like an N95 or KN95 is 83 percent less likely than non-maskers to contract circulating virus.

A person’s tolerance for risk also plays a role for how much and where they might mask, Martinello says. “It takes potentially a moment to be exposed to enough virus from a nearby person to make you sick,” he notes. Whether someone wants to avoid nearly all exposure or is comfortable taking on a little risk is an individual decision.

What is POTS? This strange disorder has doubled since the pandemic

Millions of people now live with the debilitating disorder, which can be triggered by viral illnesses like COVID-19. And many say the recommended treatment—exercise—has backfired.

(Update 10/7/2023)

In late 2021, after 18 months of long COVID symptoms, Oonagh Cousins, a member of Great Britain rowing team, was ready to resume training. She’d contracted COVID-19 in early 2020, and although her initial case was mild, Cousins spent the next year and a half experiencing a fatigue that went far beyond just feeling tired. “It was like a deep sickness,” she says, a “sludgy, deep weakness” that flared up after even mild exertion.

After that lengthy recovery period, Cousins’ only remaining symptom was a very mild case of postural orthostatic tachycardia syndrome—POTS—which is a type of dysautonomia characterized by an abnormal rise in heart rate after changing position, like sitting to standing. Patients with POTS report a variety of symptoms, including dizziness, fatigue, brain fog, and gastrointestinal disturbances.

Cousins is among  millions of people living with POTS, a number that is estimated to have doubled since the beginning of the pandemic. Some of the known triggers include pregnancy, surgery, or a viral illness, such as COVID-19. A subset of these POTS patients also has a condition called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is characterized by post-exertional malaise (PEM)—a situation in which symptoms worsen after exercise.

For patients with PEM, pushing past their physical limits—often encouraged in POTS recovery exercise protocols—can lead to major crashes. As a result, many patients with POTS and ME/CFS report being given inappropriate guidance on exercise, the consequences of which can be severe.

“They don’t teach us about ME/CFS or POTS in medical school,” says Sujana Reddy, a resident physician at East Alabama Medical Center, who developed both conditions after a COVID-19 infection in 2020.

Exercise and POTS

When Cousins felt ready to resume her training, she consulted with her doctors, who told her that the cure for her dysautonomia was exercise. With their approval, Cousins eased back into training, with three workouts a week.

After a full year of training, she had a major relapse, her dysautonomia having gone from mild to severe, which she attributes to over-training. “It was basically an accumulation of dysautonomia and post-exertional malaise,” Cousins says. As she and many other POTS patients are discovering, the relationship between exercise and dysautonomia is more complicated than the research suggests.

According to a recent estimate by the CDC, six percent of American adults are currently living with long COVID symptoms. With an estimated 79 percent of long COVID patients meeting the criteria for POTS, patients and healthcare practitioners are finding it necessary to re-evaluate how exercise fits into management of the condition.

Although exercise is considered to be a first-line treatment for POTS, in a survey of long COVID patients 89.5 percent of patients reported relapses after exertion, while other patients report difficulties with following some of the exercise protocols. As a result, the National Institute of Health and Care Excellence cautions against using graded exercise therapy for treating post-COVID fatigue. For POTS patients whose condition wasn’t triggered by a COVID-19 infection, exercise can be helpful, but as many have discovered, it’s not a cure, nor is it an effective first-line treatment. Still, many patients report being expected to prove that exercise alone is not enough to treat their symptoms, before their doctors will consider putting them on medication.

“A lot of doctors think that salt, fluid, and exercise is the only treatment patients need,” says Lauren Stiles, the founder of Dysautonomia International and a research professor in neurology at SUNY Stony Brook, who developed POTS in 2010. “That is very outdated thinking.”

When exercise backfires 

As a number of studies have shown, exercise can decrease POTS symptoms, by making the heart more efficient and encouraging the body to produce more blood. In POTS exercise protocols, patients start with cardio in a recumbent position, such as rowing, swimming, or a recumbent bike, which helps avoid triggering symptoms by avoiding an upright position. Patients also do strength-training, which helps return blood to the heart more efficiently.

However, just as with any medication, there are nuances to the benefits of exercise, whether it’s figuring out the right amount and intensity, or screening for conditions that are often associated with POTS, for which exercise may be contraindicated. For other conditions, such as ME/CFS, exercise can lead to debilitating crashes.

For one of the major studies examining the effect of exercise on POTS symptoms, of the 103 patients who finished the three-month Levine exercise protocol, 71 percent no longer met the criteria for the disorder. However, the study had a 60 percent drop-out rate, with only 103 of 251 enrolled participants completing the protocol. The study also excluded patients who had other conditions, such as autoimmune disorders, that are often found in POTS patients.

“It’s rare for me to find a patient who gets referred to me with POTS, who doesn’t also have other comorbid conditions, such as hypermobility,” says Clayton Powers, a physical therapist at the University of Utah, who specializes in treating patients with POTS.

Fitting their own needs 

Some patients have found POTS exercise programs to be useful, but only if they progress at a rate that is much slower than suggested and only if they add in medication.

For Stiles, who was a competitive snowboarder before developing POTS, exercise did not relieve her symptoms. However, after she was diagnosed and treated for an autoimmune disorder, which included regular infusions of intravenous immunoglobulin, “I went from bedridden to ice skating,” Stiles says. “Medication allowed me to very slowly work my way back into being an athletic person.”

A number of POTS patients, including many long COVID patients, also meet the criteria for ME/CFS, the hallmark symptom of which is post-exertional malaise. PEM is often characterized by a flu-like feeling, such as swollen lymph nodes, joint and muscle aches, and low-grade fevers that develop within hours and days following over-exertion.

“My world as a clinician is broken down into ‘Do you have post-exertional malaise or do you not have post-exertional malaise?’” says Todd Davenport, a physical therapy researcher at the University of the Pacific. “It’s a very important clinical decision point.”

Reddy, the resident physician in Alabama, spent the early months of her illness pushing through, only to progressively get worse. Eventually, at the urging of her doctors and family, she started physical therapy, only to experience a major crash, which left her bedbound for a month, unable to tolerate even minor stimuli such as light or sound.

For Whitney Fox, who was diagnosed with ME/CFS and POTS in 2019, even small amounts of exercise pushed her into a cycle of over-exertion followed by crashes, during which she was barely able to get out of bed. “I kept trying and trying, and I kept getting worse and worse,” Fox says.

For Lindsay Levinson, a long COVID patient with POTS and ME/CFS, understanding her new limits on exertion has been a steep learning curve, one that goes against all her former instincts. “I’m good at pushing myself,” she says. At the recommendation of her doctors, Levinson tried resuming her spinning classes, which had been her favorite activity before getting sick. After a month of doing once-a-week classes at a gentle pace, she had a massive relapse, characterized by full-body pain, and an inability to complete simple chores, such as bathing or cooking dinner.

Relapsing also kept Cousins housebound for months. After receiving treatment that includes medication, she’s been able to return to a more functional life with some gentle exercise, such as swimming laps or going for walks. “I’m trying to listen to my body, and do what my body asks for,” Cousins says. “I just want to be able to find a way to have a happy, healthy relationship with exercise, that makes me feel good.”

What causes long COVID? The answer might be in your gut

New research shows that remnants of the virus in the gut cause chronic inflammation—which may disrupt communication with the brain. Can antidepressants help?

(Update 10/23/2023)

Nearly one in five people who have had COVID-19 in the United States continue to suffer from symptoms of long COVID. But why some people recover completely while others remain sick has been a mystery. Now research has provided some enticing clues.

new study shows that bits of virus that survive in the gut cause chronic inflammation, which reduces production of serotonin—a molecule critical for communication between nerve cells in the gut and brain. The authors of the new article suggest that depletion of serotonin disrupts gut-to-brain communication, which can cause long-term neurological symptoms such as “brain fog” and impaired memory.

This may explain how “long COVID might be linked through a pathway that originates in the gut and leads to serotonin reduction,” says Christoph Thaiss, a microbiologist at the University of Pennsylvania, who led the study.

“These are very important findings that help explain why serotonin levels remain low in certain long COVID patients following SARS-CoV-2 infection,” says Liam O’Mahony, an immunologist at APC Microbiome Ireland, University College Cork, who was not involved in Thaiss’ work.

Links between the gut and brain

The brain and the gut talk to each other. In fact, the gastrointestinal nervous system with its own 500 million neurons is so large, it is sometimes called the “second brain.”

“That’s why when you’re feeling stressed, you can get abdominal pain or diarrhea,” says Kenji Hashimoto, a neuroscientist at Chiba University in Japan.

The longest of the brain nerves, called vagus nerve connects with gut and uses the neurotransmitter serotonin to communicate and regulate many biological and neurological functions such as mood, digestion, appetite, learning and memory, immune response, and heart rate, among others, says Éric Boilard, an immunologist at Laval University in Quebec City, Canada.

About 95 percent of the serotonin is produced in the gut, although the brain makes its own supply. Microbes that live in our gut also produce chemical neurotransmitters, including serotonin. While serotonin produced in the gut does not directly reach the brain, it can influence the brain via neuronal circuits through vagus nerve.

“We’ve known that the gut is a reservoir for virus for a long time,” says Melanie Gareau, a microbiologist at University of California, Davis. What is exciting is that “we’re starting to identify messengers from the gut that signal to the brain.”

Causes of neurological symptoms

Scientists have proposed several possible mechanisms that may cause long COVID. An abnormal immune response that triggers ongoing inflammation after the acute infection is one explanation, says David Sahner, a senior data adviser to National Center for Advancing Translational Sciences in Bethesda.

Previous studies had shown that fragments of SARS-CoV-2 virus that linger in patients after the initial infection heals can cause chronic inflammation, auto-antibody development, tissue damage, and in some cases disrupt communication in the nervous system.

COVID-19 also interferes with the levels of several metabolites during the initial infection. Patients not only have lower levels of serotonin but these imbalances can persist in those with long COVID.

Thaiss and his colleagues set out to find if and how all these factors are related?

They began by comparing the level of metabolites in blood samples of long COVID patients and healthy volunteers. They found that serotonin levels in blood were so different, they could predict whether a patient had fully recovered or had developed long COVID.

The long COVID patients also had changes in the blood levels of amino acids—the building blocks of proteins—compared to healthy patients. One, called tryptophan, stood out, because it was suppressed in long COVID patients. Humans need tryptophan from food to produce serotonin. That suggests that chronic inflammation caused by viral remnants lowers absorption of tryptophan from food, which then lowers blood serotonin.

Thaiss’ team also confirmed that some long COVID patients continue to excrete bits of SARS-CoV-2 virus in their stool even months after recovering from COVID-19. These remnants of the virus, called a viral reservoir, trigger the immune system to release virus fighting proteins called interferons. The extended release of interferons caused chronic inflammation in lab mice and in the long COVID patients.

Blocking interferon kept serotonin levels high in mice. The scientists confirmed that low absorption of tryptophan from food was the reason for low serotonin levels in virus-infected mice.

“The serotonin reduction affects the vagus nerve,” says Thaiss. Reduced serotonin levels due to viral infections in mice disrupted their vagus nerve signaling and mice failed to distinguish new objects from familiar ones in tests. This failure mimics neurological symptoms, such as brain fog, generally associated with long COVID in humans.

Some common antidepressant drugs, called selective serotonin reuptake inhibitors (SSRIs), such as Prozac and Sarafem boost mood by increasing serotonin in the brain. When scientists gave Prozac to sick mice, it improved their performance in recognition tests. Supplementing the mouse food with tryptophan, which improved levels of serotonin, also helped.

This new research identifies mechanisms that contribute to depleted blood levels of serotonin, says O’Mahony.

“I think we have a few actionable items about long COVID, that we can now look at in clinical trials,” says Thaiss.

Can boosting serotonin levels treat long COVID?

The new study suggests SSRI’s might be useful in treating, or even preventing long-COVID. When scientists gave Prozac to the lab mice—whose neurological symptoms mimicked long COVID because of viral infection—it restored their memory loss.

study that has not yet been peer reviewed, shows that COVID patients already on SSRI had 25 percent less risk of developing long-COVID.

“Initiating use of SSRIs prior to diagnosis of COVID-19 may be effective in reducing the risk of long-COVID,” says Hythem Sidky, a computational biologist, who led the study for the National COVID Cohort Collaborative (N3C) at the National Institutes of Health.

But whether SSRIs can cure long COVID, “remains to be determined,” says Sahner, who co-led the N3C study with Sidky.

Further research is needed to establish which serotonin boosting drug and at what dosage may help in treatment of long COVID. Fluvoxamine, an SSRI known under the brand names Luvox and Faverin, which is prescribed to treat major depressive disorder, obsessive–compulsive disorder, and post-traumatic stress disorder did not prevent long COVID although it prevented severe COVID-19 at higher doses.

“Giving fluvoxamine at a dose of 50 milligrams twice a day during acute infection did not prevent the development of long-COVID,” says Carolyn Bramante, an internist at University of Minnesota, Minneapolis. Bramante led a trial that followed overweight or obese patients for 10 more months after treating their original COVID-19 infection with fluvoxamine. “It did prevent severe COVID at a higher dose,” says Bramante. “But high doses are complicated with this drug.”

In the meantime, scientists warn patients against self-medicating with antidepressants to treat long COVID. If the levels of serotonin in brain become too high, it can cause serotonin syndrome—a rare but serious condition with symptoms such as seizures, irregular heartbeat, and unconsciousness.

“We’re going to need several ways to both prevent long-COVID and treat it,” says Bramante. “But people should only act in connection with their physician and in ways that are supported by data.”

Now we know how COVID attacks your heart

Even patients with mild COVID symptoms could face a higher risk of developing heart disease and stroke

(Update 11/8/2023)

A human heart, showing the arteries and veins which supply blood to the cardiac muscles. The blood vessels, which lie immediately below the surface of the heart, have been injected with a dye, making visible even the smallest capillaries that form this exquisite arterial network. 

Scientists have noticed that COVID-19 can trigger serious cardiovascular problems, especially among older people who have a buildup of fatty material in their blood vessels. But now a new study has revealed why and shown that SARS-CoV-2, the virus that causes COVID-19, directly infects the arteries of the heart.

The study also found that the virus can survive and grow inside the cells that form plaque—the buildup of fat-filled cells that narrow and stiffen the arteries leading to atherosclerosis. If the plaque breaks, it can block blood flow and cause a heart attack or a stroke. The SARS-CoV-2 infection makes the situation worse by inflaming the plaque and increasing the chance that it breaks free. 

This can explain long-term cardiovascular effects seen in some, if not all, COVID-19 patients.

SARS-CoV-2 virus has already been found to infect many organs outside the respiratory system. But until now it hadn’t been shown to attack the arteries.

“No one was really looking if there was a direct effect of the virus on the arterial wall,” says Chiara Giannarelli, a cardiologist at NYU Langone Health, in New York, who led the study. Giannarelli noted that her team detected viral RNA—the genetic material in the virus—in the coronary arteries. “You would not expect to see [this] several months after recovering from COVID.”

Mounting evidence now shows that SARS-CoV-2 is not only a respiratory virus, but it can also affect the heart and many other organ systems, says Ziyad Al-Aly, a clinical epidemiologist at Washington University in St. Louis. Al-Aly’s research has shown that the risk of developing heart and cardiovascular diseases, including heart failure, stroke, irregular heart rhythms, cardiac arrest, and blood clots increases two to five times within a year of COVID-19, even when the person wasn’t hospitalized.

“This important study links, for the first time, directly the SARS-CoV-2 virus with atherosclerotic plaque inflammation,” says Charalambos Antoniades, chair of cardiovascular medicine at the University of Oxford, United Kingdom.

Virus triggers the inflammation in plaque

A recent study of more than 800,000 people led by Fabio Angeli, a cardiologist at University of Insubria in Varese, Italy, has shown that COVID-19 patients develop high blood pressure twice as often as others. More worrying is that the risk of cardiac diseases can also rise for patients who suffered only mild COVID symptoms.

“I saw a patient who now has a defibrillator, and she didn’t even have a severe [COVID] illness,” says Bernard Gersh, a cardiologist at Mayo Clinic, Rochester, Minnesota.

Wondering whether the cardiovascular damage during COVID was due to the virus directly attacking the blood vessels, the NYU team analyzed autopsied tissue from the coronary arteries and plaque of older people who had died from COVID-19. They found the virus was present in the arteries regardless of whether the fatty plaques were big or small.

“The original finding in this study is that the virus was convincingly found in the plaque in the coronary artery,” says Juan Carlos Kaski, a cardiovascular specialist at St George’s, University of London, who was not involved in the study.

The NYU team found that in the arteries, the virus predominantly colonized the white blood cells called macrophages. Macrophages are immune cells that are mobilized to fight off an infection, but these same cells also absorb excess fats—including cholesterol from blood. When microphages load too much fat, they change into foam cells, which can increase plaque formation.

To confirm that the virus was indeed infecting and growing in the cells of the blood vessels, scientists obtained arterial and plaque cells—including macrophages and foam cells—from healthy volunteers. Then they grew these cells in the lab in petri dishes and infected them with SARS-CoV-2.

Giannarelli found that although virus infected macrophages at a higher rate than other arterial cells, it did not replicate in them to form new infectious particles. But when the macrophages had become loaded with cholesterol and transformed into foam cells, the virus could grow, replicate, and survive longer.

“We found that the virus tended to persist longer in foam cells,” says Giannarelli. That suggests that foam cells might act as a reservoir of SARS-CoV-2. Since more fatty buildup would mean a greater number of foam cells, plaque can increase the persistence of the virus or the severity of COVID-19.

Scientists found that when macrophages and foam cells were infected with SARS-CoV-2 they released a surge of small proteins known as cytokines, which signal the immune system to mount a response against a bacterial or viral infection. In arteries, however, cytokines boost inflammation and formation of even more plaque.

“We saw that there was a degree of inflammation [caused] by the virus that could aggravate atherosclerosis and cardiovascular events,” says Giannarelli.

These findings also confirm previous reports that measuring inflammation in the blood vessel wall can diagnose the extent of long-term cardiovascular complications after COVID-19, says Antoniades.

“What this study has found is that plaque rupture can be accelerated and magnified by the presence of the virus,” says Kaski.

Understanding heart diseases after COVID

While this new research clearly shows that SARS-CoV-2 can infect, grow, and persist in the macrophages of plaques and arterial cells, more studies are needed to fully understand the many ways COVID-19 can alter cardiac health.

“The NYU study identifies one potential mechanism, especially the viral reservoir, to explain the possible effects” says Gersh. “But It’s not going to be the only mechanism.”

This study only analyzed 27 samples from eight elderly deceased patients, all of whom already had coronary artery disease and were infected with the original strains of virus. So, the results of this study do not necessarily apply to younger people without coronary artery disease; or to new variants of the virus, which cause somewhat milder disease, says Angeli.

“We do not know if this will happen in people who have been vaccinated,” says Kaski. “There are lots of unknowns.”

It is also not clear whether and to what extent the high inflammatory reaction observed in the arteries of patients within six months after the infection, as shown in the new study, will last long-enough to trigger new plaque formation. “New studies are needed to show the time-course of the resolution of vascular inflammation after the infection,” says Antoniades.

COVID patients should watch for any new incidence of shortness of breath with exertion, chest discomfort, usually with exertion, palpitations, loss of consciousness; and talk to their physician about possible heart disease.

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