This is yet another article about the COVID-19 Virus. While I have several articles already on the virus, I am finding that some of my articles are becoming too unwieldy as I continue to update the as new information becomes available. So as more and more variants appear I have decided to write an article just discussing the variants. I will continue to update my two part flagship covid posting and my vaccine posting as well.
Table of Contents
–SARS-CoV-2 Variant Classifications and Definitions
–What’s the concern about the new COVID-19 variants? Are they more contagious?
–COVID Variants: What You Should Know
–WHO labels new Covid strain, named omicron, a ‘variant of concern,’ citing possible increased reinfection risk
–What are the Covid variants and will vaccines still work?
–There’s Always Going To Be Another Variant
–Why you shouldn’t panic over the Omicron variant
-How bad is Omicron? What scientists know so far
-Beyond Omicron: what’s next for COVID’s viral evolution
–Most Who Took COVID Vax will be dead by the year 2025.
-COVID-19 variants will keep coming until everyone can access vaccines
-Omicron’s feeble attack on the lungs could make it less dangerous
-The Omicron Variant: Mother Nature’s COVID-19 Vaccine?
-Is Omicron really less severe than Delta? Here’s what the science says.
-Omicron thwarts some of the world’s most-used COVID vaccines
-Deltacron: the story of the variant that wasn’t
SARS-CoV-2 Variant Classifications and Definitions
Viruses like SARS-CoV-2 continuously evolve as changes in the genetic code (genetic mutations) occur during replication of the genome. A lineage is a genetically closely related group of virus variants derived from a common ancestor. A variant has one or more mutations that differentiate it from other variants of the SARS-CoV-2 viruses. As expected, multiple variants of SARS-CoV-2 have been documented in the United States and globally throughout this pandemic. To inform local outbreak investigations and understand national trends, scientists compare genetic differences between viruses to identify variants and how they are related to each other.
- Mutation: A mutation refers to a single change in a virus’s genome (genetic code). Mutations happen frequently, but only sometimes change the characteristics of the virus.
- Lineage: A lineage is a group of closely related viruses with a common ancestor. SARS-CoV-2 has many lineages; all cause COVID-19.
- Variant: A variant is a viral genome (genetic code) that may contain one or more mutations. In some cases, a group of variants with similar genetic changes, such as a lineage or group of lineages, may be designated by public health organizations as a Variant of Concern or a Variant of Interest due to shared attributes and characteristics that may require public health action.
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- Genetic lineages of SARS-CoV-2 have been emerging and circulating around the world since the beginning of the COVID-19 pandemic.
- SARS-CoV-2 genetic lineages in the United States are routinely monitored through epidemiological investigations, virus genetic sequence-based surveillance, and laboratory studies.
- On November 30, 2021, the U.S. government SARS-CoV-2 Interagency Group (SIG) classified Omicron as a Variant of Concern (VOC). This classification was based on the following:
- Detection of cases attributed to Omicron in multiple countries, including among those without travel history.
- Transmission and replacement of the Delta variant in South Africa.
- The number and locations of substitutions in the spike protein.
- Available data for other variants with fewer substitutions in the spike protein that indicate a reduction in neutralization by sera from vaccinated or convalescent individuals.
- Available data for other variants with fewer substitutions in the spike protein that indicate reduced susceptibility to certain monoclonal antibody treatments.
- The SIG Variant classification scheme defines four classes of SARS-CoV-2 variants:
- Variant Being Monitored (VBM)
- Alpha (B.1.1.7 and Q lineages)
- Beta (B.1.351 and descendent lineages)
- Gamma (P.1 and descendent lineages)
- Epsilon (B.1.427 and B.1.429)
- Eta (B.1.525)
- Iota (B.1.526)
- Kappa (B.1.617.1)
- Mu (B.1.621, B.1.621.1)
- Zeta (P.2)
- Variant of Interest (VOI)
- Variant of Concern (VOC)
- Delta (B.1.617.2 and AY lineages)
- Omicron (B.1.1.529)
- Variant of High Consequence (VOHC)
- Variant Being Monitored (VBM)
- To date, no variants of high consequence have been identified in the United States.
- Vaccines approved and authorized for use in the United States are effective against the predominant variant circulating in the United States and effective therapeutics are available. CDC continues to monitor all variants circulating within the United States.
How Variants Are Classified
The U.S. Department of Health and Human Services (HHS) established a SARS-CoV-2 Interagency Group (SIG) to enhance coordination among CDC, National Institutes of Health (NIH), Food and Drug Administration (FDA), Biomedical Advanced Research and Development Authority (BARDA), and Department of Defense (DoD). This interagency group is focused on the rapid characterization of emerging variants and actively monitors their potential impact on critical SARS-CoV-2 countermeasures, including vaccines, therapeutics, and diagnostics.
The SIG meets regularly to evaluate the risk posed by SARS-CoV-2 variants circulating in the United States and to make recommendations about the classification of variants. This evaluation is undertaken by a group of subject matter experts who assess available data, including variant proportions at the national and regional levels and the potential or known impact of the constellation of mutations on the effectiveness of medical countermeasures, severity of disease, and ability to spread from person to person. Given the continuous evolution of SARS-CoV-2 and our understanding of the impact of variants on public health, variants may be reclassified based on their attributes and prevalence in the United States.
- Variants being monitored (VBM)– View current VBM in the United States that continue to be monitored and characterized by federal agencies
- Variant of interest (VOI)– Currently, no SARS-CoV-2 variants are designated as VOI
- Variant of Concern (VOC)– View current VOC in the United States that are being closely monitored and characterized by federal agencies
- Variant of high consequence (VOHC)– Currently, no SARS-CoV-2 variants are designated as VOHC
Notes: Each variant classification includes the possible attributes of lower classes (for example, VOC includes the possible attributes of VOI); variant status might escalate or deescalate based on emerging scientific evidence. This page will be updated as needed to show the variants that belong to each class. The World Health Organization (WHO) external icon also classifies variant viruses as variants of concern and variants of interest; U.S. classifications may differ from those of WHO because the impact of variants may differ by location. To assist with public discussions of variants, WHO proposed using labels consisting of the Greek alphabet (for example, alpha, beta, gamma) as a practical way to discuss variants for non-scientific audiences. The labels assigned to each variant are provided in the tables below.
CDC monitors all variants circulating in the United States. Variants designated as VBM include those where data indicates there is a potential or clear impact on approved or authorized medical countermeasures or that have been associated with more severe disease or increased transmission but are no longer detected, or are circulating at very low levels, in the United States. These variants do not pose a significant and imminent risk to public health in the United States.
A Variant of Interest or a Variant of Concern may be downgraded to this list after a significant and sustained reduction in its national and regional proportions over time, or other evidence indicates that a variant does not pose significant risk to public health in the United States.
These variants continue to be closely monitored to identify changes in their proportions and new data are continually being analyzed. If the data indicate that a VBM warrants more concern, the classification will be changed based on the SIG assessment of the attributes of the variant and the risk to public health in the United States.
Variant of Interest (VOI)
A variant with specific genetic markers that have been associated with changes to receptor binding, reduced neutralization by antibodies generated against previous infection or vaccination, reduced efficacy of treatments, potential diagnostic impact, or predicted increase in transmissibility or disease severity.
Possible attributes of a Variant of Interest:
- Specific genetic markers that are predicted to affect transmission, diagnostics, therapeutics, or immune escape.
- Evidence that it is the cause of an increased proportion of cases or unique outbreak clusters.
- Limited prevalence or expansion in the US or in other countries.
A Variant of Interest might require one or more appropriate public health actions, including enhanced sequence surveillance, enhanced laboratory characterization, or epidemiological investigations to assess how easily the virus spreads to others, the severity of disease, the efficacy of therapeutics and whether currently approved or authorized vaccines offer protection.
Currently, no SARS-CoV-2 variants are designated as VOI.
A variant for which there is evidence of an increase in transmissibility, more severe disease (for example, increased hospitalizations or deaths), significant reduction in neutralization by antibodies generated during previous infection or vaccination, reduced effectiveness of treatments or vaccines, or diagnostic detection failures.
Possible attributes of a variant of concern:
In addition to the possible attributes of a variant of interest
- Evidence of impact on diagnostics, treatments, or vaccines
- Widespread interference with diagnostic test targets
- Evidence of substantially decreased susceptibility to one or more class of therapies
- Evidence of significantly decreased neutralization by antibodies generated during previous infection or vaccination
- Evidence of reduced vaccine-induced protection from severe disease
- Evidence of increased transmissibility
- Evidence of increased disease severity
Variants of concern might require one or more appropriate public health actions, such as notification to WHO under the International Health Regulations, reporting to CDC, local or regional efforts to control spread, increased testing, or research to determine the effectiveness of vaccines and treatments against the variant. Based on the characteristics of the variant, additional considerations may include the development of new diagnostics or the modification of vaccines or treatments.
Current variants of concern in the United States that are being closely monitored and characterized are listed below. This table will be updated when a new variant of concern is identified.Footnotes for Variants of Concern
Characteristics of Selected SARS-CoV-2 Variants
WHO Label: Delta
Pango Lineage: B.1.617.2 and AY lineages (Pango lineageexternal icon)a
Spike Protein Substitutions: T19R, (V70F*), T95I, G142D, E156-, F157-, R158G, (A222V*), (W258L*), (K417N*), L452R, T478K, D614G, P681R, D950N
Nextstrain clade (Nextstrainexternal icon)b: 21A/S:478K
First Identified: India
- Increased transmissibility29
- Nearly all lineages designated as Delta are susceptible to Emergency Use Authorization (EUA) monoclonal antibody treatments. AY.1 and AY.2 lineages are not susceptible to some monoclonal antibody treatments.7, 14
- Reduction in neutralization by post-vaccination sera21
WHO Label: Omicron
Pango Lineage: B.1.1.529 (Pango lineageexternal icon)a
Spike Protein Substitutions: A67V, del69-70, T95I, del142-144, Y145D, del211, L212I, ins214EPE, G339D, S371L, S373P, S375F, K417N, N440K, G446S, S477N, T478K, E484A, Q493R, G496S, Q498R, N501Y, Y505H, T547K, D614G, H655Y, N679K, P681H, N764K, D796Y, N856K, Q954H, N969K, L981F
Nextstrain clade (Nextstrainexternal icon)b: 21K
First Identified: South Africa
- Potential increased transmissibility
- Potential reduction in neutralization by some EUA monoclonal antibody treatments
- Potential reduction in neutralization by post-vaccination sera
A VOHC has clear evidence that prevention measures or medical countermeasures (MCMs) have significantly reduced effectiveness relative to previously circulating variants.
Possible attributes of a variant of high consequence:
In addition to the possible attributes of a variant of concern
- Impact on MCMs
- Demonstrated failure of diagnostic test targets
- Evidence to suggest a significant reduction in vaccine effectiveness, a disproportionately high number of infections in vaccinated persons, or very low vaccine-induced protection against severe disease
- Significantly reduced susceptibility to multiple EUA or approved therapeutics
- More severe clinical disease and increased hospitalizations
A variant of high consequence would require notification to WHO under the International Health Regulations, reporting to CDC, an announcement of strategies to prevent or contain transmission, and recommendations to update treatments and vaccines.
Currently, no SARS-CoV-2 variants are designated as VOHC.
What’s the concern about the new COVID-19 variants? Are they more contagious?
Viruses constantly change through mutation. When a virus has one or more new mutations it’s called a variant of the original virus. Currently, one variant of the virus (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) is creating concern in the U.S.
- Delta (B.1.617.2). This variant is now the most common COVID-19 variant in the U.S. It’s nearly twice as contagious as earlier variants and might cause more severe illness. The greatest risk of transmission is among unvaccinated people. People with vaccine breakthrough infections also may spread COVID-19 to others. However, it appears that vaccinated people spread COVID-19 for a shorter period than do unvaccinated people. This variant also might reduce the effectiveness of some monoclonal antibody treatments and the antibodies generated by a COVID-19 vaccine.
In addition, the World Health Organization has classified the new variant omicron as a variant of concern. Omicron has been found in several countries. However, it’s not yet clear if omicron spreads more easily or causes more severe disease than other variants, such as delta. Research is underway.
The alpha, gamma and beta variants continue to be monitored but are spreading at much lower levels in the U.S. The mu variant is also being monitored.
While research suggests that COVID-19 vaccines are slightly less effective against the variants, the vaccines still appear to provide protection against severe COVID-19. For example:
- Early research from the U.K. suggests that, after full vaccination, the Pfizer-BioNTech COVID-19 vaccine is 88% effective at preventing symptomatic COVID-19 virus caused by the delta variant. The vaccine is 96% effective at preventing severe disease with the COVID-19 virus caused by the delta variant. The research also showed that the vaccine is 93% effective at preventing symptomatic COVID-19 virus caused by the alpha variant.
- Early research from Canada suggests that, after one dose, the Moderna COVID-19 vaccine is 72% effective at preventing symptomatic COVID-19 virus caused by the delta variant. One dose of the vaccine is also 96% effective at preventing severe disease with the COVID-19 virus caused by the delta variant.
- The Janssen/Johnson & Johnson COVID-19 vaccine is 85% effective at preventing severe disease with the COVID-19 virus caused by the delta variant, according to data released by Johnson & Johnson.
To strengthen protection against COVID-19 and circulating variants, the CDC recommends additional doses and booster doses of COVID-19 vaccines in specific instances:
- Additional dose. The CDC recommends a third dose of an mRNA COVID-19 vaccine for some people with weakened immune systems, such as those who have had an organ transplant. People with weakened immune systems might not develop enough immunity after vaccination with two doses of an mRNA COVID-19 vaccine. An additional dose might improve their protection against COVID-19.The third dose should be given at least 28 days after a second dose of an mRNA COVID-19 vaccine. The additional dose should be the same brand as the other two mRNA COVID-19 vaccine doses you were given. If the brand given isn’t known, either brand of mRNA COVID-19 vaccine can be given as a third dose.
- Booster dose. The CDC recommends a booster dose for some people who are fully vaccinated and whose immune response weakened over time. If you are age 18 or older, you have been given both doses of the Pfizer-BioNTech COVID-19 vaccine or the Moderna COVID-19 vaccine and it’s been at least 6 months, you can get a single booster dose. If you are age 18 or older, you have been given one dose of the Janssen/Johnson & Johnson COVID-19 vaccine and it’s been at least 2 months, you also can get a single booster dose. You may choose which vaccine you get as a booster dose. You can get a booster dose that is the same brand as your previous shot or shots or choose a different brand.
COVID Variants: What You Should Know
In December 2020, news media reported a new variant of the coronavirus that causes COVID-19, and since then, other variants have been identified and are under investigation. The new variants raise questions: Are people more at risk for getting sick? Will the COVID-19 vaccines still work? Are there new or different things you should do now to stay safe?
Stuart Ray, M.D., vice chair of medicine for data integrity and analytics, and Robert Bollinger, M.D., M.P.H., Raj and Kamla Gupta professor of infectious diseases, are experts in SARS-CoV-2, the virus that causes COVID-19. They talk about what is known about these new variants, and answer questions and concerns you may have.
Coronavirus Mutation: Why does the coronavirus change?
Variants of viruses occur when there is a change — or mutation — to the virus’s genes. Ray says it is the nature of RNA viruses such as the coronavirus to evolve and change gradually. “Geographic separation tends to result in genetically distinct variants,” he says.
Mutations in viruses — including the coronavirus causing the COVID-19 pandemic — are neither new nor unexpected. Bollinger explains: “All RNA viruses mutate over time, some more than others. For example, flu viruses change often, which is why doctors recommend that you get a new flu vaccine every year.”
What is the delta variant?
Since the beginning of the COVID-19 pandemic, the SARS-CoV-2 coronavirus that causes COVID-19 has mutated (changed), resulting in different variants of the virus. One of these is called the delta variant (arising from Pango lineage B.1.617.2). The delta coronavirus is considered a “variant of concern” by the WHO and CDC because it appears to be more easily transmitted from one person to another. As of September 2021, delta is regarded as the most contagious form of the SARS-CoV-2 coronavirus so far.
Here is what you should know:
The CDC recommends that everyone wait until they are fully vaccinated for COVID-19 before traveling internationally. Traveling internationally if you are not fully vaccinated for COVID-19 is not recommended, because it puts you at risk for coronavirus infection, including the SARS-CoV-2 delta variant. This includes unvaccinated children.
- Delta rapidly became the dominant variant of the SARS-CoV-2 virus in the U.S. in 2021.
- Delta variant SARS-CoV-2, the virus that causes COVID-19, is now in most countries where SARS-CoV-2 is circulating, and people traveling internationally are likely to encounter it.
- Unvaccinated adults and children should strictly follow mask, distancing and hygiene safety precautions and avoid international travel if possible.
- Being fully vaccinated for COVID-19 can protect you from the delta variant, but breakthrough infections sometimes occur.
- All three of the F.D.A.-authorized COVID-19 vaccines can protect you from the delta variant. For Pfizer and Moderna vaccines, you need both doses for maximum protection. People should know that vaccines are very effective at preventing the most severe forms of COVID-19, but breakthrough infections can occur and caution is still warranted after becoming vaccinated.
- While the authorized COVID-19 vaccines are not perfect, they are highly effective against serious coronavirus disease and reduce the risk of hospitalization and death.
- Other vaccines available in other countries may not be as effective in protecting you from the delta variant and other mutations of the coronavirus.
- Although vaccines afford very high protection, infection with the delta and other variants remain possible. Fortunately, vaccination, even among those who acquire infections, appears to prevent serious illness, hospitalization and death from COVID-19.
How many strains of COVID are there?
“We are seeing multiple variants of the SARS-CoV-2 coronavirus that are different from the version first detected in China,” Ray says.
“Different variants have emerged in England, Brazil, California and other areas. More infectious variants such as beta, which first appeared in South Africa, may have increased ability to re-infect people who have recovered from earlier versions of the coronavirus, and also be somewhat resistant to some of the coronavirus vaccines in development. Still, vaccines currently used appear to offer significant protection from severe disease caused by coronavirus variants.”
What is a variant of concern?
Coronavirus variants are classified in different categories by organizations such as the World Health Organization (WHO) and the Centers for Disease Control and Prevention (CDC).
A variant of interest is a coronavirus variant that, compared to earlier forms of the virus, has genetic characteristics that predict greater transmissibility, evasion of immunity or diagnostic testing or more severe disease.
A variant of concern has been observed to be more infectious, more likely to cause breakthrough or re-infections in those who are vaccinated or previously infected. These variants are more likely to cause severe disease, evade diagnostic tests, or resist antiviral treatment. Alpha, beta, gamma, and delta variants of the SARS-CoV-2 coronavirus are classified as variants of concern.
A variant of high consequence is a variant for which current vaccines do not offer protection. As of now, there are no SARS-CoV-2 variants of high consequence.
Will the COVID-19 vaccines work on the new variants?
Ray says, “There is evidence from laboratory studies that some immune responses driven by current vaccines could be less effective against some of these variants. The immune response involves many components, including B cells that make antibodies and T cells that can react to infected cells, and a reduction in one does not mean that the vaccines will not offer protection.
“People who have received the vaccines should watch for changes in guidance from the CDC [Centers for Disease Control and Prevention], and continue with coronavirus safety precautions to reduce the risk of infection, such as mask wearing, physical distancing and hand hygiene.”
“We deal with mutations every year for flu virus, and will keep an eye on this coronavirus and track it,” says Bollinger. “If there would ever be a major mutation, the vaccine development process can accommodate changes, if necessary,” he explains.
How are the new coronavirus variants different?
“There’s evidence that some genetic changes in SARS-CoV-2 can result in a more contagious variant,” Bollinger says. “This is particularly true for the delta variant.”
He notes that some of the mutations seem to affect the coronavirus’s spike protein, which covers the outer coating of SARS-CoV-2 and give the virus its characteristic spiny appearance. These proteins help the virus attach to human cells in the nose, lungs and other areas of the body.
“Researchers have preliminary evidence that some of the new variants seem to bind more tightly to our cells” Bollinger says. “This appears to make some of these new strains ‘stickier’ due to changes in the spike protein and therefore more easily transmitted.”
Are coronavirus variants more dangerous?
Bollinger says that some of these mutations may enable the coronavirus to spread faster from person to person, and more infections can result in more people getting very sick or dying. In addition, studies are underway to determine whether some variants could be associated with more severe disease.
“Therefore, it is very important for us to expand the number of genetic sequencing studies to keep track of these variants,” he says.
Bollinger explains that it may be more advantageous for a respiratory virus to evolve so that it spreads more easily. On the other hand, mutations that make a virus more deadly may not give the virus an opportunity to spread efficiently. “If we get too sick or die quickly from a particular virus, the virus has less opportunity to infect others. However, as we have seen with delta, more infections from a faster-spreading variant will lead to more hospitalizations and deaths,” he notes.
Could a new COVID-19 variant affect children more frequently than earlier strains?
Ray says that widespread infection with the delta variant has resulted in an increased number of cases in children, including uncommon severe infections and deaths.
“There is no convincing evidence that any of the variants have special propensity to infect or cause disease in children. We need to be vigilant in monitoring such shifts, but we can only speculate at this point,” he says.
Will there be more new coronavirus variants?
Yes. As long as the coronavirus spreads through the population, mutations will continue to happen, and the delta variant family continues to evolve.
“New variants of the SARS-CoV-2 virus are detected every week,” Ray says. “Most come and go — some persist but don’t become more common; some increase in the population for a while, and then fizzle out. When a change in the infection pattern first pops up, it can be very hard to tell what’s driving the trend — changes to the virus, or changes in human behavior. It is worrisome that similar changes to the spike protein are arising independently on multiple continents.”
Are there additional COVID-19 precautions for the new coronavirus variants?
Bollinger says that as of now, none of the new coronavirus variants call for any new prevention strategies. “We need to continue doing the basic precautions that we know work to interrupt spread of the virus,” he says.
Ray concurs: “There is no demonstration yet that these variants are biologically different in ways that would require any change in current recommendations meant to limit spread of COVID-19,” he says. “Nonetheless, we must continue to be vigilant for such phenomena. For now, the greater infectiousness we’re seeing means we must redouble our efforts using the preventative tools that we have in a multi-layered approach.”
Ray stresses that both vaccination and human behavior are important. “It is striking to note that the majority of COVID-19 deaths are now occurring in unvaccinated people, even when most adults in the USA have been vaccinated,” he says.
“The more people who are unvaccinated and infected, the more chances there are for mutations to occur. Limiting the spread of the virus through maintaining COVID-19 safeguards (mask wearing, physical distancing, practicing hand hygiene and getting vaccinated) gives the virus fewer chances to change. It also reduces the spread of more infectious variants, if they do occur.
“Vaccines are the medical miracle of 2020, but we need to re-emphasize basic public health measures, including masking, physical distancing, good ventilation indoors and limiting gatherings of people in close proximity with poor ventilation. We give the virus an advantage to evolve when we congregate in more confined spaces,” he says.
Regarding coronavirus variants, how concerned should we be?
“Most of the genetic changes we see in this virus are like the scars people accumulate over a lifetime — incidental marks of the road, most of which have no great significance or functional role,” Ray says. “When the evidence is strong enough that a viral genetic change is causing a change in the behavior of the virus, we gain new insight regarding how this virus works. The virus seems to have some limitations in its evolution – the advantageous mutations are drawn from a relatively limited menu – so there is some hope that we might not see variants that fully escape our vaccines.
“Updated versions of the current vaccines are being evaluated, but there is no clinical trial evidence yet that variant-specific vaccines would provide significantly greater protection. Though SARS-CoV-2 is changing gradually, it’s still much less genetically diverse than influenza.”
“As far as these variants are concerned, we don’t need to overreact,” Bollinger says. “But, as with any virus, changes are something to be watched, to ensure that testing, treatment and vaccines are still effective. The scientists will continue to examine new versions of this coronavirus’s genetic sequencing as it evolves.”
“In the meantime, we need to continue all of our efforts to prevent viral transmission and to vaccinate as many people as possible, and as soon as we can.”
WHO labels new Covid strain, named omicron, a ‘variant of concern,’ citing possible increased reinfection risk
The World Health Organization on Friday assigned the Greek letter omicron to a newly identified Covid variant in South Africa.
The U.N. health agency recognized the strain, first referred to as lineage B.1.1.529, as a variant of concern.
Health experts are deeply concerned about the transmissibility of the omicron variant given that it has an unusual constellation of mutations and a profile that is different from other variants of concern.
“Omicron, B.1.1.529, is named as a variant of concern because it has some concerning properties,” Maria Van Kerkhove, the WHO’s technical lead on Covid-19, said in a video published on Twitter. “This variant has a large number of mutations, and some of these mutations have some worrying characteristics.”
Experts fear that the sharp upswing of Covid cases in South Africa’s Gauteng province — where the heavily mutated strain of the virus was first identified — could mean it has greater potential to escape prior immunity than other variants. The number of omicron cases “appears to be increasing” in almost all of South Africa’s provinces, the WHO reported.
The organization only labels Covid strains as variants of concern when they’re more transmissible, more virulent or more adept at eluding public health measures, including vaccines and therapeutics. Data presented at a briefing Thursday hosted by South Africa’s Department of Health indicates that some of omicron’s mutations are connected with improved antibody resistance, which could reduce the protection offered by vaccines.
Certain mutations could also make omicron more contagious, while others haven’t been reported until now, preventing researchers from understanding how they could impact the strain’s behavior, according to a presentation at the briefing.
“Preliminary evidence suggests an increased risk of reinfection with this variant, as compared to other VOCs,” the WHO said in a statement released Friday.
The designation of a new variant of concern coupled with mounting alarm from health officials sent global markets into a tailspin Friday. Oil prices and travel and leisure stocks took heavy losses on the news.
WHO has said it will take weeks to understand how the variant may affect diagnostics, therapeutics and vaccines.
South African scientist Tulio de Oliveira said at a media briefing Thursday that the omicron variant contains around 50 mutations but more than 30 of these are in the spike protein, the region of the protein that interacts with human cells prior to cell entry.
What’s more, the receptor binding domain — the part of the virus that first makes contact with our cells — has 10 mutations, far greater than just two for the delta Covid variant, which spread rapidly earlier this year to become the dominant strain worldwide.
This level of mutation means it most likely came from a single patient who could not clear the virus, giving it the chance to genetically evolve. The same hypothesis was proposed for the Covid variant alpha.
“There’s a lot of work that is ongoing in South Africa and in other countries to better characterize the variant itself in terms of transmissibility, in terms of severity and any impact on our countermeasures, like the use of diagnostics, therapeutics or vaccines,” Van Kerkhove said. “So far there’s little information, but those studies are underway.”
Around 100 omicron variant genomes have been identified in South Africa, mostly in the Gauteng province. The variant has also been detected in Israel, Botswana and Hong Kong.
Many of the mutations identified in the omicron variant are linked to increased antibody resistance, which may reduce the effectiveness of vaccines and affect how the virus behaves with regard to inoculation, treatments and transmissibility, health officials have said.
Passengers wait at Frankfurt Airport.Boris Roessler | picture alliance | Getty Images
“There are two approaches to what happens next: Wait for more scientific evidence, or act now and row back later if it wasn’t required,” said Sharon Peacock, professor of public health and microbiology at the University of Cambridge.
“I believe that it is better to ‘go hard, go early and go fast’ and apologise if mistaken, than to take an academic view that we need to reach a tipping point in evidence before action is taken. Rapid spread in South Africa could be due to super-spreader events or other factors. But there are sufficient red flags to assume the worst rather than hope for the best — and take a precautionary approach,” Peacock said.
The European Union, the U.K., Israel, Singapore and the U.S. are among the countries imposing travel restrictions on southern African nations.
The WHO has cautioned countries against hastily imposing travel restrictions, saying they should instead take a “risk-based scientific approach.”
South Africa’s foreign ministry said Friday morning that the U.K.’s decision to take precautionary measures “seems to have been rushed as even the WHO is yet to advise on the next steps.”
What are the Covid variants and will vaccines still work?
A new heavily mutated version of coronavirus has been found that scientists say is of “great concern”.
One of most pressing questions is will vaccines still work?
What is this new variant?
There are thousands of different types, or variants, of Covid circulating across the world. That’s to be expected because viruses mutate all the time.
But this new variant, called B.1.1.529 or Omicron, has experts particularly worried because it is very different to the original Covid, which current vaccines were designed to fight.
It has a long list of genetic changes – 50 in all. Of these, 32 are in the spike protein of the virus – the part which is the target of vaccines.
However, it is too soon to know how much of a threat it poses.
Will vaccines still work?
Current vaccines are not an ideal match so might not work quite as well, say experts.
But that doesn’t mean they’ll offer zero protection.
Remember, vaccines are still very effective at protecting lives by cutting the risk of severe illness against other major Covid variants, including Delta, Alpha, Beta and Gamma.ADVERTISEMENT
Doctors say it is vital people get the recommended number of doses to gain maximum protection against existing and emerging variants.
In the UK, booster jabs are recommended for:
- Frontline health and social care workers
- Older adults in residential care homes
- People aged 16-49 years old with underlying health conditions which put them at greater risk of severe Covid
- Adults who share a household with vulnerable people
More than 16m booster or third doses have been given so far in the UK.
Although Covid infections have been rising again across the UK, the number of hospitalisations and deaths has remained well below the levels seen in earlier waves. Experts say this is because of the success of the vaccine programme.
Scientists will be running lots of tests to check if the vaccines will hold up against this latest variant.
It is early days, but experts will study potentially important mutations that might make it more infectious and able to sidestep some of the protection given by vaccines.
And they will assess if it is causing more serious disease than other variants.
How quickly could we get new vaccines against variants?
Updated versions of vaccines against Covid variants are already being designed and tested, in case they are needed at some point.
Should that time arrive, a new vaccine could be ready within weeks, to run checks on.
Manufacturers could scale up production quickly too and regulators have already discussed how to fast track the approval process.
No corners would be cut, but the whole process – from design to approval – could be much faster than when Covid vaccines were first launched.
What about the other variants?
Officials have a close watch on a few.
The most potentially dangerous ones are called variants of concern and include:
- Delta (B.1.617.2), first identified in India and now the most common type circulating in the UK
- Alpha (B.1.1.7), first identified in the UK but which spread to more than 50 countries
- Beta (B.1.351), first identified in South Africa but which has been detected in at least 20 other countries, including the UK
- Gamma (P.1), first identified in Brazil but which has spread to more than 10 other countries, including the UK
UK officials are also keeping an eye on a recent descendent of the Delta variant, called AY.4.2 or “Delta plus”.
How dangerous are variants?
There is no evidence that any of them cause more serious illness for the vast majority of people.
As with original Covid, the risk remains highest for people who are elderly or have significant underlying health conditions.
But even so, if a variant is more infectious it will lead to more deaths in an unvaccinated population.
Vaccines offer high protection against severe illness with Covid-19, including infections caused by variants of concern. The shots also reduce the risk of infection. But they do not completely eliminate all risk.
The advice to avoid infection remains the same for all strains: wash your hands, keep your distance, wear a face covering in crowded places and be vigilant about ventilation.
Why are variants occurring?
Viruses make carbon copies of themselves to reproduce but they aren’t perfect at it. Errors can creep in that change the genetic blueprint, resulting in a new version or variant.
If this gives the virus a survival advantage, the new version will thrive.
The more chances coronavirus has to make copies of itself in us – the host – the more opportunities there are for mutations to occur.
That’s why keeping infections down is important. Vaccines help by cutting transmission as well as protecting against serious Covid illness.
Experts say it is possible that the new highly altered variant B.1.1.529 may have originated in a patient whose immune system was unable to get rid of a Covid infection quickly, giving the virus more time to morph.
There’s Always Going To Be Another Variant
Just when you thought it was safe to live your life again, a new coronavirus variant has emerged. “Omicron,” the fifteenth letter of the Greek alphabet and thirteenth iteration of COVID-19, which conspicuously skipped over the letter “Xi”, threatens to keep us all locked down just a little bit longer to “slow the spread” and “flatten the curve” while public health officials do their darnedest to eradicate the virus, which they will never succeed at doing because there will always be another variant.
Viruses mutate. Viruses that contain RNA as their genetic material, such as coronaviruses and influenza, mutate even more than others. There are four species of influenza, each comprising dozens of subtypes and hundreds of subtype combinations. Despite widespread annual vaccinations and the best efforts of public health experts, influenza continues to spread, as it has since antiquity, and to kill upwards of 650,000 people each year.
At least some part of COVID-19 appears to have originated in bats, making eradication even less likely. As Michael Osterholm, an epidemiologist at the University of Minnesota, explained to the scientific journal Science, “There is no disease in the history of humankind that has disappeared from the face of the Earth when zoonotic disease was such an important part of, or played a role in, the transmission.” In other words, COVID-19—like influenza and the coronaviruses that cause the common cold—is here to stay.
Even if biology had not fated endless COVID variants, politics would have. Powerful interests in elected government, the administrative state, and putatively private enterprise seized upon the coronavirus to grow their wealth and power. So despite a low infection fatality rate, widespread vaccines, and effective treatments, our cynical ruling class has every incentive to prolong the sense of crisis.
“I think we need to just get our mindset that the virus is still in control,” warns William Schaffner, an epidemiologist at the University of Minnesota. “I don’t care about your COVID fatigue.” But the virus is not in control of anything; people are. In the old American republic, the people controlled the government through their elected representatives within boundaries set by the Constitution. In the new American oligarchy, unaccountable technocrats restructure society according to their own whims no matter what the people want, and they justify their rule by the dubious claim that they represent “science.”
The more COVID mutates, the more the symptoms remain the same: cough, fever, and the loss of our rights and way of life, which unlike our senses of smell and taste will not return once we have recovered from the virus. Biological science ensures that the “omicron” variant will become the “pi,” then the “rho,” then the “sigma,” and so on. Political science ensures that our rulers will exploit each new variant to maintain the power they’ve already taken, to scare the people into submission, and to seize whatever else they can squeeze out of us.
Why you shouldn’t panic over the Omicron variant
The new variant of concern has a large number of mutations and is spreading fast. But experts say there are many unknowns, and that vaccines and masks are still the best available protections.
Experts warned that regions with low vaccination rates could allow the virus that causes COVID-19 to evolve more rapidly, possibly yielding a more transmissible or antibody-resistant variant that would escalate the pandemic. Now this prediction may have come true.
Last week the World Health Organization named a new SARS-CoV-2 variant Omicron and classified it as a variant of concern, along with Alpha, Beta, Gamma, and Delta. The variant was discovered in South Africa, where just 23 percent of the population is vaccinated, due in part to most supplies going to North America and Europe. However, at this early stage there is still a lot scientists can’t say for sure about Omicron and its potential to worsen the COVID-19 pandemic. So far most breakthrough cases involving this variant seem to be mild, and it’s unclear how much the mutations will erode vaccine efficacy. It is also unknown whether Omicron will cause more severe illness than Delta.
Preliminary evidence from South Africa suggests that Omicron might be more transmissible than previous variants: Positive cases in the Tshwane region of Gauteng Province—where Omicron was first detected on November 9—increased from less than one percent to more than 30 percent of collected samples in the past three weeks. Omicron now makes up 76 percent of all SARS-CoV-2 sequenced in South Africa, making it the most prevalent variant in the country. It is replacing other variants faster than Delta replaced Beta.
“[It is] a reminder we have this new variant as a result of failure to control infections,” says Ravi Gupta, a clinical microbiologist at the University of Cambridge who is one of the world’s leading researchers on COVID-19.
Omicron shares many key mutations with previous variants of concern, but it has also accumulated a dozen novel mutations on its spike protein, the part of the virus that is essential for infecting human cells. The new variant has 32 mutations in this region overall, and scientists fear the large number might diminish the ability of existing antibodies to neutralize the variant, making current vaccines less effective.
“It has mutations at virtually every site that current antibodies would bind to,” says Michael Worobey, who studies the evolution of viruses at the University of Arizona. There are also mutations that could make Omicron infect cells faster and transmit from person to person more easily. “This one is worrying, and I’ve not said that since Delta,” says Gupta.
“While we know there are many mutations, in the case of this [Omicron] variant, we don’t yet know what their overall effect is,” cautions Kei Sato, a virologist at the University of Tokyo. Only about 1,000 people have been diagnosed with Omicron, and scientists currently have very few samples and genetic sequences from South Africa, which makes it difficult for experts to draw firm conclusions about Omicron’s contagiousness and whether it causes more severe disease.
On the bright side, antibodies taken from people who were first naturally infected and then vaccinated were still able to neutralize a synthetic Omicron-type virus in the laboratory. That suggests a booster dose of an mRNA vaccine may still provide robust protection against Omicron.
Omicron “is a cause for concern, not a cause for panic,” U.S. President Joe Biden said in a press briefing on Monday morning. “The best protection against this new variant or any of the various out there, the ones we’ve been dealing with already, is getting fully vaccinated and getting a booster shot.”
For now, “we have every indication that the vaccines are still effective in preventing severe disease and or complications,” says Ian Sanne, an infectious diseases specialist at University of Witwatersrand in Johannesburg, South Africa. “The data, however, is small and early.”
Omicron’s worrisome mutations
When an individual encounters the SARS-CoV-2 virus, the body’s immune cells produce antibodies that target the spike protein, the part the virus uses to attach to the ACE2 receptor protein on human cells and infect them. When antibodies bind to the spike, the virus is blocked from entering the cell. Because the spike is essential for infection, all currently authorized vaccines use it to train the body’s immune response.
The 32 mutations that occur in Omicron’s spike gene can be organized into three groups, depending on how they alter the function of the spike protein, says Olivier Schwartz, a virologist and immunologist at the Pasteur Institute in France.
Some mutations enhance the spike protein’s ability to bind to the human ACE2 receptor; some help the surface of the virus fuse with the cell and allow the virus to enter; others alter the appearance of the spike protein, making it harder to recognize and allowing the virus to evade antibodies.
Of the many mutations on Omicron’s spike, the loss of amino acids at positions 69 and 70 makes the virus twice as infectious as the original virus. But in a stroke of luck, these two mutations are not present in Delta, making Omicron easy to distinguish in a widely used PCR assay.
The University of Cambridge’s Gupta has previously shown that these deleted amino acids, along with a third mutation at position 796 on the spike protein, are associated with Alpha’s ability to evade the body’s immune response. This suggests these same three mutations could help Omicron escape existing immunity either from vaccines or previous infections—and some preliminary evidence suggests that is happening.
“To date there have been a number of breakthrough infections, but they have been mild,” says Barry Schoub, a virologist and adviser on COVID-19 vaccines to South Africa’s government. However, experts say it is too early to know whether Omicron causes more severe disease as there is a lag between infection and hospitalization.
Another cluster of mutations in Omicron at positions 655, 679 and 681 of the spike protein are thought to help the virus infect human cells more easily; they also exist in the Mu variant and are known to enhance its transmissibility.
Additionally, in a study not yet peer reviewed, researchers suggest that a mutation that Omicron shares with Alpha and Mu might help it replicate faster and resist immunity. And a mutation at the 501 position also found in Alpha, Beta, and Gamma makes the spike protein attach more tightly to the ACE2 receptor, making the virus more efficient at infecting cells.
“We see this virus spreading pretty rapidly in a population with, we think, very high levels of immunity,“ says Richard Lessells, infectious diseases specialist at the University of KwaZulu-Natal in Durban, South Africa. “That’s what gives us concern,” he adds. “[Omicron] could have kind of more immune evasion than previous variants.”
In the Gauteng region of South Africa, blood samples suggest 80 percent of the population already had some immunity because of encounters with previous SARS-CoV-2 variants. That’s why experts are worried about the rapid rise of Omicron, which accounted for 76 percent of cases in just a couple of weeks. By comparison, it took Delta several months to reach that level of prevalence.
The number of COVID-19 hospitalizations in South Africa has also risen sharply within the last month, but whether that is due to overall numbers of people becoming infected or due to specific infection with Omicron is not yet clear.
“There’s not enough information available yet to make a conclusion about the severity of Omicron in comparison to other variants,” says Ben Cowling, an epidemiologist at the University of Hong Kong. That’s because most early cases are among university students and younger people, who generally develop more mild disease.
With current data, it’s also not clear whether the growth advantage of Omicron over Delta is because of its ability to escape immunity by reinfecting previously immune people, or by infecting individuals who haven’t been exposed to the virus, notes Tom Wenseleers, an evolutionary biologist and biostatistician at the KU Leuven University in Belgium.
While the number of people testing positive in areas of South Africa affected by Omicron has risen sharply, there is not enough data to conclude whether that is entirely due to Omicron or to superspreader events among students and young people.
Despite the worrying rise in cases, preliminary data, including studies from Theodora Hatziioannou’s lab in New York, suggest that vaccines and boosters are still powerful tools against the virus.
Researchers led by Hatziioannou, of the Rockefeller University in New York, created a synthetic version of the virus that contained many of the spike protein mutations that Omicron carries. They found that neutralizing antibodies from people who had recovered from COVID-19 and then got an mRNA vaccine dose were able to fend off the mutated synthetic virus.
However, it takes between two and three weeks after infection for COVID-19 to develop and the severity of the disease to be gauged, explains Sanne, which means it will take time to determine whether the existing vaccines hold up against Omicron in the real world.
In the meantime, the best way to avoid any type of infection from Omicron or any other variant is to get more people vaccinated and for governments to continue promoting public health measures such as social distancing and mask wearing. “Please get vaccinated and boosted and mask up in public, as the mutations in this virus likely result in high-level escape from neutralizing antibodies,” says Gupta.
“The primary way to minimize the emergence of new variants is to limit ongoing transmissions,” adds Ridhwaan Suliman, a senior researcher at the Council for Scientific and Industrial Research in South Africa. “Viruses can’t mutate if they can’t replicate.”
How bad is Omicron? What scientists know so far
COVID researchers are working at breakneck speed to learn about the variant’s transmissibility, severity and ability to evade vaccines.
Barely a week has elapsed since scientists in Botswana and South Africa alerted the world to a fast-spreading SARS-CoV-2 variant now known as Omicron. Researchers worldwide are racing to understand the threat that the variant — now confirmed in more than 20 countries — poses to the world. Yet it might take scientists weeks to paint a more complete picture of Omicron, and to gain an understanding of its transmissibility and severity, as well as its potential to evade vaccines and cause reinfections.Heavily mutated Omicron variant puts scientists on alert
“Wherever I go, everyone says: tell us more about Omicron,” says Senjuti Saha, a molecular microbiologist and director of the Child Health Research Foundation in Dhaka, Bangladesh. “There is so little understanding of what’s going on, and that’s true, even for scientists.”
Nature rounds up what scientists know so far about the Omicron variant.
How fast is Omicron spreading?
Omicron’s rapid rise in South Africa is what worries researchers most, because it suggests the variant could spark explosive increases in COVID-19 cases elsewhere. On 1 December, South Africa recorded 8,561 cases, up from the 3,402 reported on 26 November and several hundred per day in mid-November, with much of the growth occurring in Gauteng Province, home to Johannesburg.
Epidemiologists measure an epidemic’s growth using R, the average number of new cases spawned by each infection. In late November, South Africa’s National Institute for Communicable Diseases (NICD) in Johannesburg determined that R was above 2 in Gauteng. That level of growth was last observed in the early days of the pandemic, Richard Lessels, an infectious-disease physician at KwaZulu-Natal University in Durban, South Africa, told a press briefing last week.
Gauteng’s R value was well below 1 in September — when Delta was the predominant variant and cases were falling — suggesting that Omicron has the potential to spread much faster and infect vastly more people than Delta, says Tom Wenseleers, an evolutionary biologist at the Catholic University of Leuven in Belgium. Based on the rise in COVID-19 cases and on sequencing data, Wenseleers estimates that Omicron can infect three to six times as many people as Delta, over the same time period. “That’s a huge advantage for the virus — but not for us,” he adds.
Researchers will be watching how Omicron spreads in other parts of South Africa and globally to get a better read on its transmissibility, says Christian Althaus, a computational epidemiologist at the University of Bern, Switzerland. Heightened surveillance in South Africa could cause researchers to overestimate Omicron’s fast growth. But if this pattern is repeated in other countries, it would be very strong evidence that Omicron has a transmission advantage, adds Althaus. “If it doesn’t happen, for example, in European countries, it means things are a bit more complex and strongly depend on the immunological landscape. So we have to wait.”
Although genome sequencing is needed to confirm Omicron cases, some PCR tests can pick up a hallmark of the variant that distinguishes it from Delta. On the basis of this signal, there are preliminary indications that cases, although extremely low in number, are rising in the United Kingdom. “That’s certainly not what we want to see right now and suggests that Omicron could indeed also have a transmission advantage in the UK,” Althaus adds.
Can Omicron overcome immunity from vaccines or infection?
The variant’s swift rise in South Africa hints that it has some capacity to evade immunity. Around one-quarter of South Africans are fully vaccinated, and it’s likely that a large fraction of the population was infected with SARS-CoV-2 in earlier waves, says Wenseleers, based on heightened death rates since the start of the pandemic.
In this context, Omicron’s success in southern Africa might be due largely to its capacity to infect people who recovered from COVID-19 caused by Delta and other variants, as well as those who’ve been vaccinated. A 2 December preprint1 from researchers at the NICD found that reinfections in South Africa have increased as Omicron has spread. “Unfortunately, this is the perfect environment for immune-escape variants to develop,” says Althaus.
How well the variant spreads elsewhere might depend on factors such as vaccination and previous infection rates, says Aris Katzourakis, who researches viral evolution at the University of Oxford, UK. “If you throw it into the mix in a highly vaccinated population that has given up on other control measures, it might have the edge there.”Omicron-variant border bans ignore the evidence, say scientists
Researchers want to measure Omicron’s ability to evade immune responses and the protection they offer. For instance, a team led by Penny Moore, a virologist at the NICD and the University of the Witwatersrand in Johannesburg, is measuring the ability of neutralizing, or virus-blocking, antibodies triggered by previous infection and vaccination to stop Omicron from infecting cells. To test this in the laboratory, her team is making ‘pseudovirus’ particles — an engineered version of HIV that uses SARS-CoV-2’s spike protein to infect cells — that match Omicron, which harbours as many as 32 changes to spike.
Another South Africa-based team, led by virologist Alex Sigal at the Africa Health Research Institute in Durban, is conducting similar tests of virus-neutralizing antibodies using infectious SARS-CoV-2 particles. So is a team led by Pei-Yong Shi, a virologist at the University of Texas Medical Branch in Galveston, who is collaborating with the makers of the Pfizer–BioNTech vaccine to determine how it holds up against Omicron. “I was really very concerned when I saw the constellation of mutations in the spike,” he says. “We just have to wait for the results.”
Previous studies of Omicron’s spike mutations — particularly in the region that recognizes receptors on human cells — suggest that the variant will blunt the potency of neutralizing antibodies. For instance, in a September 2021 Nature paper2, a team co-led by Paul Bieniasz, a virologist at Rockefeller University in New York City, engineered a highly mutated version of spike — in a virus incapable of causing COVID-19 — that shares numerous mutations with Omicron. The ‘polymutant spike’ proved fully resistant to neutralizing antibodies from most of the people they tested, who had either received two doses of an mRNA vaccine or recovered from COVID-19. With Omicron, “we expect there to be a significant hit”, says Bieniasz.
How will vaccines fare against Omicron?
If Omicron can dodge neutralizing antibodies, it does not mean that immune responses triggered by vaccination and prior infection will offer no protection against the variant. Immunity studies suggest that modest levels of neutralizing antibodies may protect people from severe forms of COVID-19, says Miles Davenport, an immunologist at the University of New South Wales in Sydney, Australia.
Other aspects of the immune system, particularly T cells, may be less affected by Omicron’s mutations than are antibody responses. Researchers in South Africa plan to measure the activity of T cells and another immune player called natural killer cells, which might be especially important for protection against severe COVID-19, says Shabir Madhi, a vaccinologist at the University of the Witwatersrand.
Madhi, who has led COVID-19 vaccine trials in South Africa, is also part of efforts to conduct epidemiological studies of vaccines’ effectiveness against Omicron. There are anecdotal reports of breakthrough infections involving all three vaccines that have been administered in South Africa — Johnson & Johnson, Pfizer–BioNTech and Oxford–AstraZeneca. But Madhi says researchers will want to quantify the level of protection against Omicron provided by vaccines, as well as by previous infection.
He suspects that the results will be reminiscent of how the AstraZeneca–Oxford vaccine performed against the Beta variant, an immune-evading variant that was identified in South Africa in late 2020. A trial led by Madhi found that the vaccine offered little protection against mild and moderate disease, while a real-world analysis in Canada showed greater than 80% protection against hospitalization.
If Omicron behaves similarly, Madhi says, “we’re going to see a surge of cases. We’re going to see lots of breakthrough infections, lots of reinfections. But there’s going to be this unhinging of the case rate in the community compared to the hospitalization rate”. Early reports suggest that most breakthrough infections with Omicron have been mild, says Madhi. “For me, that is a positive signal.”
Will current boosters improve protection against Omicron?
The threat of Omicron has prompted some rich countries, such as the United Kingdom, to accelerate and broaden the roll-out of COVID vaccine booster doses. But it’s not yet clear how effective these doses will be against this variant.
Third doses supercharge neutralizing-antibody levels, and it’s likely that this will provide a bulwark against Omicron’s ability to evade these antibodies, says Bieniasz. His team’s work on the polymutant spike found that people who had recovered from COVID-19 months before receiving their jabs had antibodies capable of blocking the mutant spike. To Bieniasz, those results suggest that people with repeated exposure to SARS-CoV-2’s spike protein, be it through infection or a booster dose, are “quite likely to have neutralizing activity against Omicron”.
Does Omicron cause milder or more severe disease than previous variants?
Early reports linked Omicron with mild disease, raising hopes that the variant might be less severe than some of its predecessors. But these reports — which are often based on anecdotes or scant scraps of data — can be misleading, cautions Müge Çevik, an infectious-disease specialist at the University of St Andrews, UK. “Everyone is trying to find some data that could guide us,” she says. “But it’s very difficult at the moment.”
A major challenge when assessing a variant’s severity is how to control for the many confounding variables that can influence the course of disease, particularly when outbreaks are geographically localized. For example, reports of mild disease from Omicron infection in South Africa could reflect the fact that the country has a relatively young population, many of whom have already been exposed to SARS-CoV-2.
During the early days of the Delta outbreak, there were reports that the variant was causing more serious illness in children than did other variants — an association that dissolved once more data were collected, Çevik says.
Researchers will be looking for data on Omicron infections in other countries. This geographical spread, and a larger sample size as cases accrue, will give researchers a better idea of how generalizable the early reports of mild disease might be. Ultimately, researchers will want to conduct case-controlled studies, in which two groups of participants are matched in terms of important factors such as age, vaccination status and health conditions. Data from both groups will need to be collected at the same time, because the number of hospitalizations can be influenced by overall hospital capacity in a region.
And, crucially, researchers will need to control for the level of economic deprivation. A rapidly spreading new variant may reach vulnerable groups more rapidly, Çevik says, by nature of their work or living conditions. And such groups often experience more severe disease.
All of this will take time. “I think the severity question will be one of the last bits that we’ll be able to untangle,” she says. “That’s how it happened with Delta.”
Where has Omicron spread and how are scientists tracking it?
More countries are detecting the Omicron variant, but the capacity to rapidly sequence viruses from positive COVID-19 tests is concentrated in wealthy countries, meaning that early data on Omicron’s spread will be skewed.
Surveillance efforts in Brazil and some other countries are taking advantage of a distinctive result on a particular PCR test that could allow them to pinpoint potential Omicron cases for sequencing, says virologist Renato Santana at the Federal University of Minas Gerais in Brazil. The test looks for segments of three viral genes, one of which is the gene that encodes for the spike protein. Mutations in Omicron’s spike gene prevent its detection in the test, meaning that samples containing the variant will test positive for only two of the genes.
Even so, not everyone uses that test and it could take some time before Omicron’s spread is fully mapped. Despite some guidelines urging countries to sequence 5% of their samples that test positive for SARS-CoV-2, few can afford to do so, says computational virologist Anderson Brito at the All for Health Institute in São Paulo, Brazil. And Brito worries that the travel bans enacted by some countries against South Africa, and other southern African nations, in the wake of its Omicron discovery could discourage governments from sharing genomic surveillance data. “We are punishing those who did a good job,” he says.
In Bangladesh, which sequences about 0.2% of positive coronavirus samples, researchers would be eager to ramp up sequencing to keep tabs on Omicron and other emerging variants, says Saha. But resources are limited. Bangladesh is recovering from a large dengue outbreak, she adds. “In the global south, we are all worried about COVID, but let’s not forget our endemic diseases,” Saha says. “We can only do so many.”
Beyond Omicron: what’s next for COVID’s viral evolution
The rapid spread of new variants offers clues to how SARS-CoV-2 is adapting and how the pandemic will play out over the next several months
As the world sped towards a pandemic in early 2020, evolutionary biologist Jesse Bloom gazed into the future of SARS-CoV-2. Like many virus specialists at the time, he predicted that the new pathogen would not be eradicated. Rather, it would become endemic — the fifth coronavirus to permanently establish itself in humans, alongside four ‘seasonal’ coronaviruses that cause relatively mild colds and have been circulating in humans for decades or more.
Bloom, who is based at the Fred Hutchinson Cancer Research Center in Seattle, Washington, saw these seasonal coronaviruses as potentially providing a roadmap for how SARS-CoV-2 might evolve and for the future of the pandemic. But little is known about how these other viruses continue to thrive. One of the best-studied examples — a seasonal coronavirus called 229E — infects people repeatedly throughout their lives. But it’s not clear whether these reinfections are the result of fading immune responses in their human hosts or whether changes in the virus help it to dodge immunity. To find out, Bloom got hold of decades-old blood samples from people probably exposed to 229E, and tested them for antibodies against different versions of the virus going back to the 1980s.
The results were striking1. Blood samples from the 1980s contained high levels of infection-blocking antibodies against a 1984 version of 229E. But they had much less capacity to neutralize a 1990s version of the virus. They were even less effective against 229E variants from the 2000s and 2010s. The same held true for blood samples from the 1990s: people had immunity to viruses from the recent past, but not to those from the future, suggesting that the virus was evolving to evade immunity.
“Now that we’ve had almost two years to see how SARS-CoV-2 evolves, I think there are clear parallels with 229E,” says Bloom. Variants such as Omicron and Delta carry mutations that blunt the potency of antibodies raised against past versions of SARS-CoV-2. And the forces propelling this ‘antigenic change’ are likely to grow stronger as most of the planet gains immunity to the virus through infection, vaccination or both. Researchers are racing to characterize the highly mutated Omicron variant. But its rapid rise in South Africa suggests that it has already found a way to dodge human immunity.How bad is Omicron? What scientists know so far
How SARS-CoV-2 evolves over the next several months and years will determine what the end of this global crisis looks like — whether the virus morphs into another common cold or into something more threatening such as influenza or worse. A global vaccination push that has delivered nearly 8 billion doses is shifting the evolutionary landscape, and it’s not clear how the virus will meet this challenge. Meanwhile, as some countries lift restrictions to control viral spread, opportunities increase for SARS-CoV-2 to make significant evolutionary leaps.
Scientists are searching for ways to predict the virus’s next moves, looking to other pathogens for clues. They are tracking the effects of the mutations in the variants that have arisen so far, while watching out for new ones. They expect SARS-CoV-2 eventually to evolve more predictably and become like other respiratory viruses — but when this shift will occur, and which infection it might resemble is not clear.
Researchers are learning as they go, says Andrew Rambaut, an evolutionary biologist at the University of Edinburgh, UK. “We haven’t had much to go on.”
An early plateau
Scientists tracking the evolution of SARS-CoV-2 are looking out for two broad categories of changes to the virus. One makes it more infectious or transmissible, for instance by replicating more quickly so that it spreads more easily through coughs, sneezes and wheezes. The other enables it to overcome a host’s immune response. When a virus first starts spreading in a new host, the lack of pre-existing immunity means that there is little advantage to be gained by evading immunity. So, the first — and biggest — gains a new virus will make tend to come through enhancements to infectivity or transmissibility.
“I was thoroughly expecting that this new coronavirus would adapt to humans in a meaningful way — and that would probably mean increased transmissibility,” says Wendy Barclay, a virologist at Imperial College London.
Genome sequencing early in the pandemic showed the virus diversifying and picking up about two single-letter mutations per month. This rate of change is about half that of influenza and one-quarter that of HIV, thanks to an error-correcting enzyme coronaviruses possess that is rare among other RNA viruses. But few of these early changes seemed to have any effect on the behaviour of SARS-CoV-2, or show signs of being favoured under natural selection.
An early mutation called D614G within the gene encoding the virus’s spike protein — the protein responsible for recognizing and penetrating host cells — seemed to offer a slight transmissibility boost2. But this gain was nothing like the leaps in transmissibility that researchers would later observe with the variants Delta and Alpha, says Sarah Otto, an evolutionary biologist at the University of British Columbia in Vancouver, Canada.
Otto sees the virus’s evolution as like walking in a landscape, where higher elevations equate to improved transmissibility. The way she sees it, when SARS-CoV-2 began spreading in humans it seemed to be on a ‘fitness plateau’ surrounded by a landscape of many possible evolutionary outcomes. In any given infection, there were probably thousands of viral particles each with unique single-letter mutations, but Otto suspects that few, if any, of these made the virus more infectious. Most changes probably reduced transmissibility.
“If the virus entered at a reasonably high point, any one-step mutation would take it downhill,” Otto says. Summiting higher peaks required the combinations of several mutations to make more-significant gains in its ability to spread.
Reaching new heights
In late 2020 and early 2021, there were signs that SARS-CoV-2 had scaled some distant peaks. Researchers in the United Kingdom spotted a variant called B.1.1.7 that contained numerous mutations in its spike protein. “It was a bit unusual because it seemed to come out of nowhere,” says Francois Balloux, a computational biologist at University College London.
That variant — since renamed Alpha — spread at least 50% faster than earlier circulating lineages. UK public-health officials linked it to a mysterious rise in cases in southeast England during a national lockdown in November 2020. Around the same time, virus hunters in South Africa linked another mutation-laden variant called B.1.351 — now known as Beta — to a second wave of infections there. Not long after, a highly transmissible variant, now called Gamma, was tracked to Amazonas state in Brazil.
These three ‘variants of concern’ share some mutations, particularly in key regions of the spike protein involved in recognizing the host-cell ACE2 receptors that the virus uses to enter cells. They also carried mutations similar or identical to those spotted in SARS-CoV-2 in people with compromised immune systems whose infections lasted for months. This led researchers to speculate that long-term infections might allow the virus to explore different combinations of mutations to find ones that are successful. Typical infections lasting days offer fewer opportunities. Super-spreading events, where large numbers of people are infected, might also explain why some variants flourished and others fizzled out.
Whatever their origins, all three variants seemed to be more infectious than the strains they displaced. But Beta and Gamma also contained mutations that blunted the potency of infection-blocking ‘neutralizing’ antibodies triggered by previous infection or vaccination. This raised the possibility that the virus was beginning to behave in the ways predicted by Bloom’s studies of 229E.
The three variants spread around the world, particularly Alpha, which sparked new waves of COVID-19 as it came to dominate in Europe, North America, the Middle East and beyond (see ‘Variant waves’). Many researchers expected that a descendant of Alpha — which seemed to be the most infectious of the bunch — would pick up additional mutations, such as those that evade immune responses, to make it even more successful. “That absolutely proved not to be the case,” says Paul Bieniasz, a virologist at Rockefeller University in New York City. “Delta came out of left field.”
The Delta dilemma
The Delta variant was identified in India’s Maharashtra state during a ferocious wave of COVID-19 that hit the country in the spring of 2021, and researchers are still taking stock of its consequences for the pandemic. Once it arrived in the United Kingdom, the variant spread quickly and epidemiologists determined that it was about 60% more transmissible than Alpha, making it several times as infectious as the first circulating strains of SARS-CoV-2. “Delta is kind of a super-Alpha,” says Barclay. “I think the virus is still looking for solutions to adapt to the human host.”
Studies from Barclay’s laboratory and others suggest that Delta made significant gains in its fitness by improving its ability to infect human cells and spread between people3,4. Compared with other variants, including Alpha, Delta multiplies faster and to higher levels in the airways of infected individuals, potentially outpacing initial immune responses against the virus.
Yet researchers expect such gains to become ever smaller. Scientists measure a virus’s inherent ability to spread in an immunologically naive population (that is, unvaccinated and not exposed to the virus previously) by a number called R0, which is the average number of people an infected person infects. Since the start of the pandemic this figure has jumped as much as threefold. “At some point, I would expect that increased transmissibility will stop happening,” says Bloom. “It’s not going to become infinitely transmissible.” Delta’s R0 is higher than seasonal coronaviruses and influenza, but still lower than that of polio or measles.
Other established human viruses do not make the leaps in infectivity that SARS-CoV-2 has in the past two years, and Bloom and other scientists expect the virus to eventually behave in the same way. Trevor Bedford, an evolutionary biologist at the Fred Hutchinson, says the virus must balance its ability to replicate to high levels in people’s airways with the need to keep them healthy enough to infect new hosts. “The virus doesn’t want to put someone in bed and make them sick enough that they’re not encountering a number of other people,” he says. One way for the virus to thread this needle would be to evolve to grow to lower levels in people’s airways, but maintain infections for a longer period of time, increasing the number of new hosts exposed to the virus, says Rambaut. “Ultimately there’s going to be trade-off between how much virus you can produce and how quickly you elicit the immune system.” By lying low, SARS-CoV-2 could ensure its continued spread.
If the virus evolved in this way, it might become less severe, but that outcome is far from certain. “There’s this assumption that something more transmissible becomes less virulent. I don’t think that’s the position we should take,” says Balloux. Variants including Alpha, Beta and Delta have been linked to heightened rates of hospitalization and death — potentially because they grow to such high levels in people’s airways. The assertion that viruses evolve to become milder “is a bit of a myth”, says Rambaut. “The reality is far more complex.”
The rise of Omicron
Delta and its descendants now account for the vast majority of COVID-19 cases worldwide. Most researchers expected these Delta lineages to eventually outcompete the last holdouts. But Omicron has undermined those predictions. “A lot of us were expecting the next weird variant to be a child of Delta, and this is a bit of a wild card,” says Aris Katzourakis, a specialist in viral evolution at the University of Oxford, UK. Teams in Botswana and South Africa identified the variant in late November — although researchers say it is unlikely to have originated in either country — and health officials have linked it to a rapidly growing outbreak centred in South Africa’s Gauteng province. The variant harbours around 30 changes to spike, many shared with the other variants of concern, and scientists worldwide are working to gauge the threat it poses.
The swift rise in cases of Omicron in South Africa suggests that the new variant has a fitness advantage over Delta, says Tom Wenseleers, an evolutionary biologist and biostatistician at the Catholic University of Leuven in Belgium. Omicron carries some of the mutations associated with Delta’s sky-high infectivity. But if increased infectivity were the sole reason for its rapid growth, it would translate to an R0 in the 30s, Wenseleers says. “That’s very implausible.”
Instead, he and other researchers suspect that Omicron’s rise may be largely due to its ability to infect people who are immune to Delta through vaccination or previous infection.
Scientists’ portrait of Omicron is still blurry and it will take weeks before they can fully assess its properties. But if the variant is spreading, in part, because of its ability to evade immunity, it fits in with theoretical predictions about how SARS-CoV-2 is likely to evolve, says Sarah Cobey, an evolutionary biologist at the University of Chicago in Illinois.
As gains in SARS-CoV-2’s infectivity start to slow, the virus will have to maintain its fitness through overcoming immune responses, says Cobey. For instance, if a mutation or set of mutations halved a vaccine’s ability to block transmission, this could vastly increase the number of available hosts in a population. Cobey says it’s hard to imagine that any future gains in infectivity could provide the same boost.
That evolutionary path, towards immune evasion and away from gains in infectivity, is common among established respiratory viruses such as influenza says Adam Kucharski, a mathematical epidemiologist at the London School of Hygiene and Tropical Medicine. “The easiest way for the virus to cause new epidemics is to evade immunity over time. That’s similar to what we see with the seasonal coronaviruses.”
Lab experiments and sequencing of circulating variants have identified a smorgasbord of mutations in the spike protein that weaken the potency of neutralizing antibodies triggered by infection and vaccination. Variants carrying these mutations, such as Beta, have blunted the effectiveness of vaccines. But they have not obliterated the protection that the shots offer, particularly against severe disease.
Compared with other variants, Omicron contains many more of these mutations, particularly in the region of spike that recognizes host cells. Preliminary analysis from Bloom suggests that these mutations might render some portions of spike unrecognizable to the antibodies raised by vaccines and previous infection with other strains. But lab experiments and epidemiological studies will be needed to fully appreciate the effects of these mutations.
Evolving to evade immune responses such as antibodies could also carry some evolutionary costs. A spike mutation that dodges antibodies might reduce the virus’s ability to recognize and bind to host cells. The receptor-binding region of spike — the major target for neutralizing antibodies — is relatively small, says Jason McLellan, a structural biologist at the University of Texas at Austin, and the region might be able to tolerate only so much change and still perform its main job of attaching itself to host cells’ ACE2 receptors.
It’s also possible that repeated exposure to different versions of spike — through infection with different virus strains, vaccine updates or both — could eventually build up a wall of immunity that SARS-CoV-2 will have difficulty overcoming. Mutations that overcome some people’s antibody responses are unlikely to foil responses across an entire population, and T-cell-mediated immunity, another arm of the immune response, seems to be more resilient to changes in the viral genome.
Such constraints might slow SARS-CoV-2’s evasion of immunity, but they are unlikely to stop it, says Bloom. There is clear evidence that some antibody-dodging mutations do not carry large evolutionary costs, says McLellan. “The virus will always be able to mutate parts of the spike.”
A virus in transition
How SARS-CoV-2 evolves in response to immunity has implications for its transition to an endemic virus. There wouldn’t be a steady baseline level of infections, says Kucharski. “A lot of people have a flat horizontal line in their head, which is not what endemic infections do.” Instead, the virus is likely to cause outbreaks and epidemics of varying size, like influenza and most other common respiratory infections do.
To predict what these outbreaks will look like, scientists are investigating how quickly a population becomes newly susceptible to infection, says Kucharski, and whether that happens mostly though viral evolution, waning immune responses, or the birth of new children without immunity to the virus. “My feeling is that small changes that open up a certain fraction of the previously exposed population to reinfection may be the most likely evolutionary trajectory,” says Rambaut.
The most hopeful — but probably least likely — future for SARS-CoV-2 would be to follow the path of measles. Infection or vaccination provides lifetime protection, and the virus circulates largely on the basis of new births. “Even a virus like measles, which has essentially no ability to evolve to evade immunity, is still around,” says Bloom.
A more likely, but still relatively hopeful, parallel for SARS-CoV-2 is a pathogen called respiratory syncytial virus (RSV). Most people get infected in their first two years of life. RSV is a leading cause of hospitalization of infants, but most childhood cases are mild. Waning immunity and viral evolution together allow new strains of RSV to sweep across the planet each year, infecting adults in large numbers, but with mild symptoms thanks to childhood exposure. If SARS-CoV-2 follows this path — aided by vaccines that provide strong protection against severe disease — “it becomes essentially a virus of kids,” says Rambaut.
Influenza offers another scenario — in fact two. The influenza A virus, which drives global seasonal influenza epidemics each year, is characterized by the rapid evolution and spread of new variants able to escape the immunity elicited by past strains. The result is seasonal epidemics, propelled largely by spread in adults, who can still develop severe symptoms. Flu jabs reduce disease severity and slow transmission, but influenza A’s fast evolution means the vaccines aren’t always well matched to circulating strains.
But if SARS-CoV-2 evolves to evade immunity more sluggishly, it might come to resemble influenza B. That virus’s slower rate of change, compared with influenza A, means that its transmission is driven largely by infections in children, who have less immunity than adults.
How quickly SARS-CoV-2 evolves in response to immunity will also determine whether — and how often — vaccines need to be updated. The current offerings will probably need to be updated at some point, says Bedford. In a preprint5 published in September, his team found signs that SARS-CoV-2 was evolving much faster than seasonal coronaviruses and even outpacing influenza A, whose major circulating form is called H3N2. Bedford expects SARS-CoV-2 to eventually slow down to a steadier state of change. “Whether it’s H3N2-like, where you need to update the vaccine every year or two, or where you need to update the vaccine every five years, or if it’s something worse, I don’t quite know,” he says.
Although other respiratory viruses, including seasonal coronaviruses such as 229E, offer several potential futures for SARS-CoV-2, the virus may go in a different direction entirely, say Rambaut and others. The sky-high circulation of the Delta variant and the rise of Omicron — aided by inequitable vaccine roll-outs to lower-income countries and minimal control measures in some wealthy countries such as the United States and the United Kingdom — offer fertile ground for SARS-CoV-2 to take additional surprising evolutionary leaps.
For instance, a document prepared by a UK government science advisory group in July raised the possibility that SARS-CoV-2 could become more severe or evade current vaccines by recombining with other coronaviruses. Continued circulation in animal reservoirs, such as mink or white-tailed deer, brings more potential for surprising changes, such as immune escape or heightened severity.
It may be that the future of SARS-CoV-2 is still in human hands. Vaccinating as many people as possible, while the jabs are still highly effective, could stop the virus from unlocking changes that drive a new wave. “There may be multiple directions that the virus can go in,” Rambaut says, “and the virus hasn’t committed.”
Most Who Took COVID Vax will be dead by the year 2025.
Most of the people who took a COVID “vaccine” will be dead by the year 2025. The proof is now available for all to see.
Thanks to the people who participated in this first ever human experiment with a mRNA gene-therapy, fooled into thinking it was a “vaccine” for a phony “pandemic” allegedly caused by the never-isolated “COVID-19,” we now know the following based on fact-based, post-vaccine research:
1.) It’s not a vaccine. The COVID-19 mRNA vaccine does not provide immunity to Covid or it’s variants so you can still catch Covid and transmit it to others making you asymptomatic. You will likely need a booster shot every 6 months, so get ready to roll up that sleeve every six months once that system rolls out.
[link to www.bustle.com]
2.) The 95% efficacy is the RRR (Relative Reduction Risk) where the real reduction rate ARR (Absolute Reduction Risk) is less than 2% as per this scientific Lancet study.
[link to www.thelancet.com]
This means you are really not protected much at all, as the architects of this phony pandemic would like you to ‘believe.’
3.) The lipid nanoparticles in the vaccines do not remain in the intramuscular region of the deltoid muscle. They seep out into the cardiovascular system infecting the entire body with spike-protein. Something the manufacturers claimed would never happen, yet it does and is why the adverse-side effects are so bad with this shot.
[link to www.sciencedirect.com]
4.) The spike-protein itself is toxic and a part of the disease pathology being the cause of inflammation, ACE2 deregulation and opens up immunity pathways. This means Myocarditis (heart inflammation), Encephalitis (brain inflammation ) and hepatomegaly (liver inflammation) are huge risks and confirmed by many adverse-reactions reported to VAERS and EuroVigilance.
This means the spike-protein itself is enough to damage the cardiovascular system and organs, some of which can have harmful events in the future and is like injecting someone with Covid-19 damaging the inside of the body rather than the lungs.
5.) The synthetic spike-protein itself has coding errors and a 5 GxxxG motif placing it in the category of a prion which could pose a long-term risk of neural degenerative diseases.
6.) The lipid nanoparticles after injection bulk in Ovaries in women followed by bone-marrow. Dr. Robert Malone the inventor of mRNA covers these findings in lay terms for stupid people who can’t process scientific data easily.
[link to www.bitchute.com]
Hal Turner Editorial Opinion
If it wasn’t for the highly uninformed and unaware folks who jumped on an experimental gene-therapy shot which skipped any real, meaningful, trials that would have presented the above findings, we now have this data and evidence from the human lab-rats running around gleefully and ignorantly celebrating their Eugenics shot, completely blind to the short-term and long term consequences that this data all points to: MOST of them will die from one or more of the conditions outlined in the reports above, and MOST of those deaths will take place by the year 2025.
Enjoy your harmful spike-protein that you will never get out of your body, and the neural degenerative, long-term risks, which ultimately could lead to untreatable deadly neurological illnesses as your brain slowly rots and deteriorates from the prion causing misfolded proteins that damage your neurons slowly over time.
Your sacrifice for the safety of others, which will likely kill most of you, was based on your ignorance, your failure to research things for yourself, and your willingness to simply accept what other (ignorant) people – like politicians – told you.
World population of 500 million coming; just as the Georgia Guide Stones suggested, and the psychotic maniacs who believe humans need to be culled from the planet, took literally.
How about we blame the real culprits who created this in the first place:
Fauci with his gain-of-function research that was banned in the US so he moved it the lab in Wuhan where this took place.
Bill Gates with his depopulation agenda and ties to pedophile Jeffery Epstein.
The CDC/WHO/Rockefeller Foundation and John Hopkins, who ran Event 201, Spars, Lockstep, planning all of this for their globalist new world order.
COVID-19 variants will keep coming until everyone can access vaccines
The emergence of Omicron underscores the consequences of vaccine inequity. Experts say it will take more than donations to fix the problem.
Angelique Coetzee was puzzled. The South African doctor had been seeing COVID-19 patients who mostly had sore throats and fevers. But on November 18 Coetzee examined a 29-year-old man complaining of extreme fatigue and severe headaches—symptoms more in line with heat stroke than COVID-19. By the end of the day, Coetzee had treated seven or eight similar cases.
“It didn’t make any sense to me,” says Coetzee, chair of the South African Medical Association.
Within a week, researchers determined that the patients were infected with a new SARS-CoV-2 variant, now known as Omicron, that has a large number of mutations and can spread more rapidly than previous variants. Omicron is now dominant in South Africa and many other countries, including the United States.
Omicron’s rise has reignited discussion about how to ensure the entire world can get a jab. The World Health Organization has set a target of vaccinating 70 percent of the global population by mid-2022. But while wealthy countries like the U.S. have already immunized more than 60 percent of their populations, vaccination in low-income countries is lagging. In South Africa only 27 percent of the population is fully vaccinated, while in Nigeria, Papua New Guinea, and Sudan that number is less than 3 percent.
The problem goes beyond supply constraints. Experts say low-income countries face massive infrastructure challenges to distribute doses quickly and widely. They argue that wealthy countries have more than just a moral obligation to help address vaccine equity, because when the virus is circulating anywhere, it has more opportunities to mutate and spread.
Mutations are normal for a virus, whose only purpose is to infect cells and replicate inside of them. In a single person’s body, the SARS-CoV-2 virus might copy its own genome at least thousands of times. Coronaviruses have so-called proofreading enzymes to keep them from introducing mistakes into their genetic code, but errors are bound to slip through, and that’s when mutations occur.
Most of these mutations are useless or even destructive to the virus, points out Wendy Barclay, a virologist at Imperial College London. She says the chance that a mutation will give an advantage to the virus, such as making it more transmissible or able to evade immunity from vaccination, is as low as 1-in-100,000. But those odds increase the more a virus is allowed to replicate.
The best way to keep new variants from arising is thus to deny the virus the opportunity to spread and replicate. That can be done by social distancing, wearing masks, and testing—but the best weapon is widespread vaccination.
“As long as Africa is not vaccinated, you will never be able to sleep soundly,” Coetzee says.
How vaccination suppresses variants
Vaccines have two main advantages: They save lives by preventing people from getting severely sick, and they help control viral replication. Breakthrough infections in vaccinated people tend to be mild, which means a sick person won’t exhale as much virus for as long as they would if they were unvaccinated. That gives the virus less time to replicate inside the body and fewer opportunities to multiply in the rest of the population.
That’s where vaccine equity comes in. Allowing a virus as transmissible as SARS-CoV-2 to run through parts of the world where large swaths of people are unvaccinated creates a real problem, says Ingrid Katz, associate faculty director at the Harvard Global Health Institute. “The only way to get in front of it is to use everything in your arsenal, and that includes vaccinating the world,” she says.
Although it’s nearly impossible to pinpoint the exact origins of a viral variant, we do know that in India, low levels of vaccination played a role in the catastrophic emergence and surge of the Delta variant earlier this year.
In early 2021 the country had begun rolling out vaccines only to those at high risk of severe disease due to their age, comorbidities, or frequent exposure to the virus. The rest of the adult population wasn’t scheduled for shots until September 2021.
“All this was based on premise that India was out of the danger zone,” says K. Srinath Reddy, president of the Public Health Foundation of India. Cases and deaths were low in mid-January, and experts were predicting that India had built up enough herd immunity to avoid another wave. Then, Reddy says, India saw a surge of travel, election rallies, and religious festivals.
“It was as though India had turned its back on the virus, though the virus had not turned its back on us,” he says.
The Delta variant was first identified in March, when less than one percent of the population of nearly 1.4 billion people was fully vaccinated. Sure enough, cases and hospitalizations surged—soon followed by a staggering loss of life.
A shaky start to vaccine supplies
Unfortunately, vaccine inequities began to build long before any COVID-19 vaccines were even approved. Wealthy countries pre-ordered hundreds of billions of doses in early deals with pharmaceutical companies—leaving low-income countries without access to the vaccines from the start.
“You set up a system of inequity right from the get-go,” Katz says.
The WHO partnered with international nonprofits to address those inequities through COVAX, an initiative to secure doses for low-income countries. But vaccines are still disproportionately going to wealthy countries as they administer booster doses.
Some countries have stepped up their donations in the name of vaccine equity, but Reddy points out that these donations have not always been well thought out. In the last year, there have been several high-profile instances in which wealthy countries waited to share their vaccine stockpiles until they were close to expiring—causing hundreds of thousands of donated doses to go to waste. For instance, South Sudan had to destroy nearly 60,000 doses in April, and up to a million doses went to waste in Nigeria in November.
“That’s not charity—that’s just dumping,” Reddy says.
Still, Amavi argues that COVAX has made an extraordinary difference in addressing vaccine equity for COVID-19 compared to past vaccination campaigns. The human papillomavirus vaccine, for example, first became available in 2006—but many African countries have only had access to it in the last couple of years.
“With COVAX we have seen that in less than one year, all COVID-19 vaccines have been made available everywhere,” Amavi says. “I think it is a great achievement to have bridged the gap between producing countries and African countries that were not receiving the vaccine in the beginning.”
The rocky road to global distribution
Once countries have secured enough doses, though, they must figure out how to distribute them. And although low-income countries might get discounts on the jabs, it costs them more than high-income countries to roll out the shots.
“It’s a challenge in Africa,” Coetzee says. “It doesn’t matter how many donations you give us.”
According to the Global Dashboard for Vaccine Equity, low-income countries would have to increase their healthcare spending by an average of nearly 57 percent to vaccinate 70 percent of their populations. That’s because many low-income countries lack the infrastructure—from electrical grid capacity to a trained healthcare workforce—to rapidly administer doses to billions of people. Distributing the mRNA vaccines is particularly daunting since they require access to cooler trucks and ultra-cold storage at healthcare facilities that are under-resourced even in the best of times.
By contrast, high-income countries only need to increase spending by less than an additional one percent to vaccinate their entire populations.
In India, the arrival of the Delta variant prompted the country to step up immunizations. Reddy says that the country has used drones to help get doses into remote areas and has launched a door-to-door vaccination campaign. India’s health minister reports that 85 percent of its eligible population has now had a first dose and more than half is fully vaccinated. However, many low-income countries simply lack the capacity to mobilize thousands of healthcare workers to go door-to-door—if they have that many trained professionals at all.
Yet another challenge is convincing people to take the vaccine. Amavi says much of the vaccine hesitancy across the world can be blamed on a COVID-19 infodemic—or the spread of misinformation and disinformation that has been sowed by the anti-vax movement.
But Katz says people in low-income countries are also understandably skeptical. She points to early reports that the Pfizer and Moderna vaccines were safer and more efficacious than those available to low-income countries, such as AstraZeneca and Johnson & Johnson.
Although this imbalance was because of cold-chain issues, Katz says it created some understandable vaccine hesitancy in countries where people feel they have gotten stuck with the worse vaccines. To remedy this, she says, public health experts must do better to reassure the population that the vaccines they’re receiving are safe and effective.
What can be done about inequities?
Solutions to vaccine inequities start at the country level. Katz says that wealthy countries can share more of their stockpiled vaccine doses or even forgo their place in line for upcoming shipments. The international community can also provide financial assistance for low-income countries to build up healthcare infrastructure—which would also help during the inevitable next pandemic.
Public health experts have also called on Moderna and Pfizer to help low-income countries produce their own mRNA vaccines—which would dramatically reduce the burdens of acquiring, transporting, and distributing them. Katz says this would require the companies not just to release their intellectual property rights but also to share their technology and raw materials.
She adds that although the Pfizer and Moderna vaccines stood out early on—proving to be more than 90 percent effective at preventing severe disease—there is promising new evidence for other vaccines.
The one-dose Johnson & Johnson vaccine, for example, was only 66.3 percent effective in its original clinical trials, but the company reported in the fall that a second dose raised the vaccine’s efficacy against moderate to severe disease caused by the original virus to 94 percent. Although the J&J shot may be less effective against newer variants, Katz argues that this data shows two doses of the jab are about as effective as the mRNA vaccines.
Barclay, too, points to new data out of the United Kingdom showing that mixing vaccines can boost immunity. A study published in The Lancet found that people who initially received two doses of the AstraZeneca vaccine had higher levels of immunity after receiving a booster of one of the six other vaccines that are available.
“So all is not lost,” she says. If countries can make progress getting the first shots in arms, they can always come back and boost with the mRNA vaccines.
Coetzee, meanwhile, advocates for developing vaccine tablets that can be administered more easily in low-income countries. Even if the mRNA vaccines could be made widely available in low-income countries, they would still need cooler trucks to transport it and enough trained medical personnel to mix the vaccine, dilute it, portion it out into a syringe, and administer doses.
“Everything can potentially lead to an error,” she says. “To give a tablet, there’s not a lot that can go wrong. You just need to make sure that the patient swallows the tablet.”
Ultimately, most experts agree that policymakers and voters everywhere need to understand that their safety is ephemeral until more of the world is vaccinated. Katz urges people to make donations, advocate within their communities, and petition their governments to do more to address vaccine equity.
“When will we learn that we have to be in collaboration globally?” she says. “We cannot go on like this.”
Coetzee agrees. She suggests that richer countries launch programs to allow their citizens to sponsor vaccines for people in low-income countries. Beyond that, she says, everyone who has access to shots can help simply by getting vaccinated, getting boosted if you’re eligible, masking up, and practicing social distancing and hand washing.
“What are you doing as a responsible citizen?” she asks. “You also need to play a role.”
Omicron’s feeble attack on the lungs could make it less dangerous
Mounting evidence from animal studies suggests that Omicron does not multiply readily in lung tissue, which can be badly damaged in people infected with other variants
Early indications from South Africa and the United Kingdom signal that the fast-spreading Omicron variant of the coronavirus SARS-CoV-2 is less dangerous than its predecessor Delta. Now, a series of laboratory studies offers a tantalizing explanation for the difference: Omicron does not infect cells deep in the lung as readily as it does those in the upper airways.
“It’s a very attractive observation that might explain what we see in patients,” says Melanie Ott, a virologist at the Gladstone Institute of Virology in San Francisco, California, who was not involved in the research. But she adds that Omicron’s hyper-transmissibility means that hospitals are filling quickly — despite any decrease in the severity of the disease it causes.
Authorities in South Africa announced on 30 December that the country had passed its Omicron peak without a major spike in deaths. And a 31 December UK government report said that people in England who were infected with Omicron were about half as likely to require hospitalization or emergency care as were those infected with Delta.
But the number of people who have gained immune protection against COVID-19 through vaccination, infection or both has grown over time, making it difficult to determine whether Omicron intrinsically causes milder disease than earlier variants. For answers, researchers have turned to animals and to cells in laboratory dishes.How the coronavirus infects cells — and why Delta is so dangerous
Michael Diamond, a virologist at Washington University in St. Louis, Missouri, and his colleagues infected hamsters and mice with Omicron and other variants to track disease progression. The differences were staggering: after a few days, the concentration of virus in the lungs of animals infected with Omicron was at least ten times lower than that in rodents infected with other variants. Other teams have also noted that compared with previous variants, Omicron is found at reduced levels in lung tissue.
Diamond says he was especially shocked to see that the Omicron-infected animals nearly maintained their body weight, whereas the others quickly lost weight — a sign that their infections were causing severe disease. “Every strain of SARS-CoV-2 has infected hamsters very easily, to high levels,” he says, “and it’s clear that this one is different for hamsters.” The lungs are where the coronavirus does much of its damage, and lung infection can set off an inflammatory immune response that ravages infected and uninfected cells alike, leading to tissue scarring and oxygen deprivation. Fewer infected lung cells could mean milder illness.
Another group found that Omicron is much less successful than previous variants at infecting lung cells and miniature lung models called organoids4. These experiments also identified a plausible player in the difference: a protein called TMPRSS2, which protrudes from the surfaces of many cells in the lungs and other organs, but is notably absent from the surfaces of most nose and throat cells.
Previous variants have exploited this protein to infect cells, but the researchers noticed that Omicron doesn’t bind to TMPRSS2 so well. Instead, it tends to enter cells when it is ingested by them.
Upper airway preferred
Difficulty entering lung cells could help to explain why Omicron does better in the upper airways than in the lungs, says Ravindra Gupta, a virologist at the University of Cambridge, UK, who co-authored one of the TMPRSS2 studies4. This theory could also explain why, by some estimates, Omicron is nearly as transmissible as measles, which is the benchmark for high transmissibility, says Diamond. If the variant lingers in the upper airways, viral particles might find it easy to hitch a ride on material expelled from the nose and mouth, allowing the virus to find new hosts, says Gupta. Other data provide direct evidence that Omicron replicates more readily in the upper airways than in the lungs.
The latest results could mean that “the virus establishes a very local infection in the upper airways and has less chance to go and wreak havoc in the lungs”, Ott says. That would be welcome news — but a host’s immune response plays an important part in disease severity, and scientists need more clinical data if they are to understand how Omicron’s basic biology influences its disease progression in humans.
Omicron’s course of infection could also have implications for children, says Audrey John, a specialist in paediatric infectious disease at the Children’s Hospital of Philadelphia in Pennsylvania. Young children have relatively small nasal passages, and babies breathe only through their noses. Such factors can make upper respiratory conditions more serious for children than for adults, John says. But she adds that she has not seen data suggesting an uptick in the numbers of young children hospitalized for croup and other conditions that could indicate a severe infection of the upper respiratory tract.
Although there is still much to learn about the new variant, Gupta says that fears raised in late November by the multitude of mutations in Omicron’s genome have not been completely borne out. He says the initial alarm offers a cautionary tale: it’s difficult to predict how a virus will infect organisms from its genetic sequence alone.
The Omicron Variant: Mother Nature’s COVID-19 Vaccine?
For several weeks, much of the world has been obsessed with the Omicron variant of the virus that causes COVID-19. What initially started as a trickle of media reports about a highly-mutated and rapidly-spreading “variant of concern” that originated in Africa quickly transformed into a global hysteria that once again closed borders, disrupted global stock markets, switched countless schools and universities to virtual learning, triggered broadening of vaccination and booster mandates, and persuaded some officials in the United States government to predict a “winter of death” and caution families not to gather over the sacred holiday period. Is this fear and isolation truly warranted?
This panic has been fueled solely by rising COVID case counts (some of which could be attributed to increased testing) coupled with the government’s and mainstream media’s addiction to fostering fear and hysteria. As both a physician and scientist, I believe it is essential that we take a measured, evidence-based approach to dealing with Omicron. And when we look at the totality of the emerging facts, there is a very real possibility that Omicron could lead us into light instead of darkness. Here’s why:
To understand why the Omicron variant could be a blessing in disguise — and possibly usher in the end of the COVID-19 pandemic by acting as Mother Nature’s vaccine — we must examine what makes this virus unique. The Omicron variant has over 26 mutations in its RNA sequence, which is a tremendous number of changes in the genetic sequence of the virus. Among these many mutations is an “insertion” where a new letter is inserted into the gene sequence. Interestingly, this sequence resembles that of another coronavirus, which causes the common cold. The Omicron variant may have picked up genetic sequences from a common cold coronavirus in someone who was infected with both viruses and, in doing so, become weakened.
Because of the enormous number of mutations, the Omicron variant is in many ways a totally new virus. It appears that it has become more transmissible (doubling in just 1-2 days), in part due to its ability to evade immunity, while becoming a lot less deadly. While the case numbers have spiked, data from South Africa and the UK have suggested that the chance of becoming very sick or dying has plummeted by 80% or higher.
Why is this so important? Because viruses compete with one another, and the Omicron variant is rapidly replacing the more dangerous Delta variant. Soon, it could become the only COVID virus around, causing no more than a bad cold in most people, particularly the vaccinated. And as it rapidly spreads throughout this holiday season as we all travel and congregate — even with vaccinations and masks — the Omicron variant is effectively giving every person it touches a type of immunity that no COVID vaccine has yet given us: a robust, possibly long-acting immunity against the entire virus, rather than just the spike protein. We know from many other vaccines that exposing the body to a weakened or attenuated version of a live virus can produce the most effective protection. Anyone who has been vaccinated against measles, mumps, rubella, rotavirus, chickenpox, smallpox, or yellow fever has actually been injected with a live, attenuated version of the very same virus that causes disease.
So, if the Omicron variant acts like a live, attenuated COVID vaccine that rapidly spreads in the air, rather than through a needle, we might very well emerge from this holiday season finally facing an end to the deadly phase of pandemic. And if you add to this the widespread availability of vaccinations for those at risk and two newly FDA-approved oral treatments for COVID-19 that can reduce hospitalization by yet another 80%, there is indeed a very bright light at the end of this long and dark tunnel. Let’s look forward to 2022 with hope and view it as an opportunity to heal, rebuild, and move on.
Is Omicron really less severe than Delta? Here’s what the science says.
This variant is more transmissible. So how do you protect yourself? And what are the implications for vaccines, masks, hygiene, and social distancing?
If you get COVID-19 in the United States right now, chances are high that it’s the Omicron variant, which now accounts for around 95 percent of the country’s reported cases. With dozens of mutations, Omicron is different from the previously dominant Delta variant in significant ways, which means that, after two years of getting a handle on how to manage risk, you might need to shift at least some of your behaviors.
Among the changes, Omicron is more transmissible and better at evading existing antibodies. “To me, the biggest shift, the most shocking thing, is how incredibly infectious this thing is. I have never seen anything so infectious in my life,” says Carlos del Rio, an epidemiologist and infectious diseases specialist Emory University in Atlanta, Georgia. At the same time, Omicron causes different symptoms and seems to lead to less severe disease.
Still, different strains of SARS-CoV-2 share important similarities, and much of the basic public health advice—get vaccinated, wear a mask—remains the same. Here’s what the latest research says about staying safe in the age of Omicron.
Is Omicron really causing less severe disease than Delta?
Multiple lines of evidence from various parts of the world suggest that the Omicron variant causes a less severe form of COVID-19. In South Africa, where Omicron was first detected in November 2021, a private health insurance administrator reported in mid-December that adults with Omicron were 29 percent less likely to be hospitalized, compared with adults infected several months earlier. In the U.K., the rate of hospital admission among people who went to the emergency room with Omicron was a third of what it was for Delta, according to a summary of research from the U.K. Health Security Agency released on December 31, 2021.
As of early January, U.S. adults with Omicron were less than half as likely to visit the emergency room, be hospitalized, or be put on a ventilator, according to preliminary work by researchers from Case Western Reserve University School of Medicine. Their study, which has not yet been peer-reviewed, examines data for more than 14,000 patients and accounts for their vaccination status and any pre-existing conditions.
A shift in symptoms reflects those trends, del Rio says. In the hospital, patients are showing up less often with pneumonia-like symptoms and hyperactive immune systems, as seen in previous waves. Instead, they’re more often presenting with congestion and scratchy throats. “In Omicron, the symptoms are more like a head cold,” he says.
Does severity differ based on age or preexisting conditions?
Omicron appears to be less severe than Delta in all age groups, even in adults older than 65 and in children too young to be vaccinated, according to the Case Western study. Still, as with other health issues, age remains a factor, del Rio says. “For any disease, if you’re older, you’re going to do a lot worse,” he says.
People with underlying conditions or compromised immune systems also remain more vulnerable, as do people who are unvaccinated. Although current vaccines are less effective at preventing symptoms from Omicron than from Delta, the U.K. report found that people who were fully boosted were up to 88 percent less likely to be hospitalized with Omicron compared with unvaccinated people. Hospitals around the country report that unvaccinated patients make up the majority of people now in intensive care units.
Regardless of age or health status, people infected with Omicron can feel terrible even if they don’t have to go to the hospital, and the variant continues to hospitalize and kill many people, emphasized Tedros Adhanom Ghebreyesus, director-general of the World Health Organization, in a virtual press conference last week.
Why is Omicron dangerous if it’s less severe than Delta?
Omicron is between two and four times more contagious than Delta, according to a Danish study that has not yet been peer reviewed. It’s also better at evading the antibodies triggered by vaccines, which is why it’s causing more breakthrough infections. As a result, more people are getting sick and showing up at hospitals, where more staff are calling in sick, del Rio says.
Omicron has 36 mutations within its spike protein, which is the part essential for anchoring the virus on human cells and infecting them. Though none are peer reviewed, at least half a dozen studies using small animal models—such as mice and hamsters—and laboratory cell cultures have started to reveal how those mutations alter the way that Omicron enters cells and replicates, says John Moore, a vaccine researcher and virologist at Weill Cornell Medicine in New York.
Unlike previous variants, Omicron appears unable to infect lung cells as efficiently, which in turn makes it less damaging and the symptoms less severe. Viral loads are significantly lower in the lungs of Omicron-infected rodents in some studies. But in the upper respiratory tract, which includes the nose and sinuses, Omicron seems to replicate more than a hundred times faster than Delta.
That mix of changes—the preference for the upper airway, better immune invasion, and high transmissibility—reflects how evolution pushes the virus to ensure its own future by replicating and spreading even when that does not make individuals sicker.
“It kind of doesn’t matter to the virus, once it’s replicated, whether that person lives or dies as long as it can get to the next host,” Moore says. “It’s all about genome replication.”
What do these changes mean for at-home testing?
All strains of the SARS-CoV-2 virus can infect cells in the mouth, and Omicron may be particularly abundant there compared with other variants, early evidence suggests. In one study that has not yet been peer reviewed, researchers in South Africa tested 382 people who were not sick enough to be hospitalized but still had COVID-19 symptoms. They found that in those with Delta, nose swabs were more accurate, but for Omicron, saliva tests worked best.
Other studies also suggest that rapid antigen tests that rely on nasal swabs might be especially slow to identify infections with Omicron. In one study posted last week that has not yet been peer reviewed, researchers looked at samples from 30 people who tested positive for COVID-19 around the United States during outbreaks in early December. For most cases of Omicron, PCR tests showed positive days before a rapid test did. Those results echo what people have been reporting on social media, says study coauthor Anne Wyllie, a medical microbiologist at the Yale School of Public Health in New Haven, Connecticut.
Given the growing evidence for Omicron’s prevalence in spit, social media has been full of DIYers and researchers advocating that people swab their throats with at-home test kits. Wyllie has even tried it herself using the swab from a rapid test. The result was negative, but she felt more confident that it was a true negative than if she’d only swabbed her nose.
“It’s not what’s been authorized by the FDA, and it’s a very tricky topic to speak out on because of that,” she says. That’s why many other experts are hesitant to recommend the off-label use. While throat swabs might eventually become part of the testing equation, rapid tests were designed for noses, not throats, says Jill Weatherhead, an infectious disease expert at the Baylor College of Medicine in Houston.
“At this point, the recommendation would be to continue to do the test as they’ve been designed to be done until further testing has been shown that it’s effective,” Weatherhead says.
Does double masking help protect against Omicron?
The Centers for Disease Control and Prevention does not currently recommend double masking or the use of specific masks. But other countries, including Austria, France, and Germany, have upgraded their guidelines to recommend medical-grade varieties, such as surgical masks or N95s. And some U.S. experts have spoken out in favor of higher quality masks.
One study found that, if fitted correctly, N95s block an average of 90 percent of exhaled particles, while surgical masks blocked 74 percent. That can make a substantial difference in community spread. In Bangladesh, an intervention boosted the percentage of people wearing surgical masks in some villages from 13 percent to 42 percent. Researchers then found an 11 percent drop in COVID-19 symptoms, with bigger gains in older groups. Evidence on cloth masks is mixed, but wearing a cloth mask over a surgical mask can block more than 85 percent of cough particles, according to some research.
Experts recommend choosing your mask based on the situation you’re in. In social situations, Moore wears a cloth mask decorated with the logo of his favorite soccer team, Liverpool. When walking around at work or in stores, he wears a thicker cloth mask that he finds comfortable. Del Rio says he wears an N95 whenever he’s with patients. But masking alone won’t protect you from Omicron, he adds. “This is not about some magic bullet, this is about a combination effect,” he says. “If you’re vaccinated and you’re boosted and you’re wearing a good-fitting mask, you can spend a lot of time with somebody.”
Do we still need to disinfect surfaces, stand further away from each other, or alter any other aspect of personal hygiene?
Like prior variants, Omicron is primarily airborne, and experts agree that wiping down surfaces is probably more trouble than it’s worth. “Transmission from surfaces is low,” Wyllie says. Given “the time, energy, money, resources and mental health put into that kind of concern—you’re better spending that on hand-washing, social distancing, and mask-wearing.“
Also, the six-foot rule is more of a reminder that being close to an infected person increases the risk of transmission, says Abraar Karan, an infectious diseases doctor at Stanford University in Palo Alto, California.
“Transmission can happen beyond six feet of distance, for sure,” he says. “However, distance makes transmission less likely, as aerosols get diluted with further distance.” Your risk also depends on ventilation, what kinds of masks people around you are wearing, and other factors.
Is long COVID still a risk when it comes to Omicron?
It’s too soon to know, and it likely will be months before researchers can tell if Omicron causes symptoms that stick around for the long-term. But some experts are hopeful that long lasting consequences will be less common because of Omicron’s tendency to stay out of the lungs, and because more people are getting vaccinated, which can help prevent infections and lower risk of developing a number of symptoms. “I would suspect we will still see cases,” Wyllie says. “But because we have far more people now vaccinated, I am hoping we see less long COVID-19.”
Omicron thwarts some of the world’s most-used COVID vaccines
Inactivated-virus vaccines elicit few, if any, infection-blocking antibodies — but might still protect against severe disease.
The world’s most widely used COVID-19 vaccines provide little to no protection against infection with the rapidly spreading Omicron variant, laboratory evidence suggests.
Inactivated-virus vaccines contain SARS-CoV-2 particles that have been chemically treated to make it impossible for them to cause an infection. Stable and relatively easy to manufacture, such vaccines have been distributed widely as part of China’s global vaccine diplomacy, helping them to become the jab of choice in many countries. But a multitude of experiments show that they are consistently hobbled by Omicron.
Many people who receive two jabs of an inactivated vaccine fail to produce immune molecules that can counter Omicron transmission. And even after a third dose of an inactivated vaccine, an individual’s levels of ‘neutralizing’ antibodies, which provide a potent safeguard against viral infection of cells, tend to remain low. A third shot of another type of vaccine, such as those based on messenger RNA or purified proteins, seems to offer better protection against Omicron.
The findings are prompting many scientists and public-health researchers to re-evaluate the role of inactivated vaccines in the global fight against COVID-19.
“At this stage, we have to evolve our ideas and adjust our vaccination strategies,” says Qiang Pan-Hammarström, a clinical immunologist at the Karolinska Institute in Stockholm.
Inactivated vaccines were instrumental in the campaign for worldwide vaccine coverage last year. They include those made by China’s Sinovac and Sinopharm, which together account for nearly 5 billion of the more than 11 billion COVID-19 vaccine doses delivered globally so far, according to numbers compiled by data-tracking firm Airfinity in London (see ‘Many shields against COVID-19’). More than 200 million doses of other inactivated shots such as India’s Covaxin, Iran’s COVIran Barekat and Kazakhstan’s QazVac have also been delivered.
Such products remain crucial for preventing hospitalization and death from COVID-19. And they can still serve a valuable immune-priming function for as-yet unvaccinated individuals.
But an early sign that inactivated vaccines might not hold up to Omicron came in December, when researchers in Hong Kong analysed blood from 25 recipients of the two-dose CoronaVac vaccine, made by the Beijing-based company Sinovac. Not a single person had detectable neutralizing antibodies against the new variant — raising the possibility that all the participants were highly vulnerable to Omicron infection.
Sinovac has disputed this finding, pointing to internal data showing that 7 out of 20 people who had received the company’s vaccine had tested positive for antibodies capable of neutralizing Omicron. Other studies involving people immunized with Covaxin, which is made by Bharat Biotech in Hyderabad, India, and BBIBP-CorV, produced by state-owned Chinese company Sinopharm, in Beijing, have also concluded that inactivated vaccines retain some potency against Omicron — although, as researchers at the Translational Health Science and Technology Institute in Faridabad, India, put it in their study, the immune responses remain “sub-optimal”. The work on Covaxin has not yet been peer reviewed.
A third dose of inactivated vaccine helps to restore neutralization activity for many individuals. A 292-person study by researchers at the Shanghai Jiao Tong University School of Medicine in China, for example, identified neutralizing antibodies against Omicron in just 8 people tested 8–9 months after an initial course of BBIBP-CorV. After another shot of the same vaccine, that number rose to 228. This work has not yet been peer reviewed. Omicron likely to weaken COVID vaccine protection
Levels of neutralizing antibodies in each person’s blood remained low. But as molecular virologist Rafael Medina at the Pontifical Catholic University of Chile in Santiago points out: “There are other parts of the immune response that are also playing a role.” T cells destroy infected cells; B cells remember past infections and strengthen immune responses for the future; and binding antibodies contribute to viral control.
In a preprint published in December, Medina and his co-authors — led by immunologist Galit Alter at the Ragon Institute of MGH, MIT and Harvard in Cambridge, Massachusetts — showed that people immunized with CoronaVac maintain non-neutralizing antibodies that both bind Omicron and assist immune cells in gobbling up infected cells.
On the defensive
Those kinds of result show that recipients of inactivated vaccines, although not necessarily protected against infection by Omicron, should still be shielded from the worst ravages of COVID-19 triggered by the variant, says Murat Akova, an infectious-disease specialist at Hacettepe University School of Medicine in Ankara.
All the same, an extra dose of vaccine could offer some much-needed immune insurance. Experiments conducted by Pan-Hammarström and her colleagues found that, after two doses of inactivated vaccine, an mRNA top-up hoists levels of binding antibodies, memory B cells and T cells. And studies of samples from China, and the United Arab Emirates have shown that a protein-based booster triggers higher numbers of neutralizing antibodies than does a third shot of an inactivated vaccine. Many of these results have not yet been peer reviewed.
But a single booster with a different type of vaccine might not be enough to subdue Omicron, warns Akiko Iwasaki, a viral immunologist at Yale School of Medicine in New Haven, Connecticut.
Iwasaki and her co-authors studied blood samples from 101 individuals who received two doses of CoronaVac followed by an mRNA booster. Before the boost, the samples showed no detectable Omicron neutralization. Afterwards, 80% of analysed samples showed some Omicron-blocking activity. But the quantities of antibodies that had Omicron-neutralizing potential were not much greater in this group than in a separate population that had received two doses of mRNA vaccine and no booster. The work has not yet been peer reviewed.
Before the Omicron variant emerged, Iwasaki had been advocating single mRNA boosters for recipients of inactivated vaccines. “We were really celebrating how wonderful this strategy is,” she says, “and then — boom! — Omicron hit.” Now, she thinks these people probably need two extra jabs.
“The bar keeps being raised by the variants,” Iwasaki says. “We’re playing catch up all the time.”
Deltacron: the story of the variant that wasn’t
News of a ‘super variant’ combining Delta and Omicron spread rapidly last week, but researchers say it never existed and the sequences may have resulted from contamination.
On 7 January, virologist Leondios Kostrikis announced on local television that his research group at the University of Cyprus in Nicosia had identified several SARS-CoV-2 genomes that featured elements of both the Delta and Omicron variants.
Named by them as ‘Deltacron,’ Kostrikis and his team uploaded 25 of the sequences to the popular public repository GISAID that evening, and another 27 a few days later. On 8 January, financial news outlet Bloomberg picked up the story, and Deltacron became international news.
The response from the scientific community was swift. Many specialists declared both on social media and to the press that the 52 sequences did not point to a new variant, and were not the result of recombination — the genetic sharing of information — between viruses, but instead probably resulted from contamination in the laboratory.
“There is no such thing as #Deltacron,” tweeted Krutika Kuppalli, a member of the World Health Organization’s COVID-19 technical team based at the Medical University of South Carolina in Charleston, on 9 January. “#Omicron and #Delta did NOT form a super variant.”
Spread of misinformation
The story behind how a small crop of SARS-CoV-2 sequences became the focus of a brief and intense scientific controversy is complicated. And although some researchers applaud the system for quickly catching a possible sequencing error, others warn that the events of last week may offer a cautionary tale on the spread of misinformation during the pandemic.
Kostrikis says that aspects of his original hypothesis have been misconstrued, and that — despite the confusing name that some of the media took to mean that the sequences were those of a Delta–Omicron recombinant virus — he never said that the sequences represented a hybrid of the two.
Nevertheless, 72 hours after the researchers uploaded the sequences, Kostrikis removed them from public view on the database, pending further investigation.
Cheryl Bennett, an official at the GISAID Foundation’s Washington DC office says that, as more than 7 million SARS-CoV-2 genomes have been uploaded to the GISAID database since January 2020, some sequencing mistakes should not come as a surprise.
“However, rushing to conclusions on data that have just been made available by labs that find themselves under significant time pressure to generate data in a timely manner is not helpful in any outbreak,” she says.
An error in the sequence?
The ‘Deltacron’ sequences were generated from virus samples obtained by Kostrikis and his team in December as part of an effort to track the spread of SARS-CoV-2 variants in Cyprus. While examining some of their sequences, the researchers noticed an Omicron-like genetic signature in the gene for the spike protein, which helps the virus to enter cells.
In an e-mail to Nature, Kostrikis explains that his initial hypothesis was that some Delta virus particles had independently evolved mutations in the spike gene similar to those common in Omicron. But after the wide news coverage, other scientists working on genetic sequencing and COVID-19 pointed out another possibility: a lab error.
Sequencing any genome depends on primers — short bits of manufactured DNA that serve as the starting point for sequencing by binding to the target sequence.
Delta, however, has a mutation in the spike gene that reduces some primers’ ability to bind to it, making it harder to sequence this region of the genome. Omicron doesn’t share this mutation, so if any Omicron particles were mixed into the sample owing to contamination, it might make the sequenced spike gene seem to be similar to that in Omicron, says Jeremy Kamil, a virologist at Louisiana State University Health Shreveport.
This type of contamination, says Kamil, is “so, so common”.
Kostrikis counters that if Deltacron was a product of contamination, sequencing should have turned up Omicron sequences with Delta-like mutations, as Omicron has its own primer-hindering mutation. He adds that the Deltacron lab contamination argument was “spearheaded by social media without considering our complete data, and without providing any real solid evidence that it is not real.”
However, other researchers have also pointed out that even if the sequences aren’t the result of contamination, the mutations identified by Kostrikis are not exclusive to Omicron and are found in other variants, making ‘Deltacron’ something of a misnomer.
In fact, GISAID is littered with sequences that have elements of sequences seen in other variants, says Thomas Peacock, a virologist at Imperial College London. Such sequences “get uploaded all the time”, he says. “But, generally, people don’t have to debunk them because there isn’t a load of international press all over them.”
“Scientists need to be very careful about what they are saying,” one virologist, who wanted to remain anonymous to avoid becoming embroiled in the controversy, told Nature. “When we say something, borders can be closed.”
Kostrikis now says he is “in the process of investigating all the crucial views expressed by prominent scientists around the world about my recent announcement”. He says he plans on submitting the research for peer review.
In the interim, Kamil and other researchers fear that such incidents could make researchers more hesitant to share time-sensitive data. “You have to allow for the scientific community to self-correct,” he says. “And, in a pandemic, you have to facilitate the rapid sharing of viral genome data, because that’s how we find variants.”
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