I have written several articles on the coronavirus and on masks. A series of links have been provided at the bottom of this article for your convenience. This article will, however address a different aspect of the virus. Links are provided for Dr. Fauci as well, because he is mentioned in this article.
Note: this article was written in the attempt to distill a massive amount of data on covid into a more manageable format. Since its first posting in July, I have updated it several times. Each time I update it I will move it up in the order of my postings to make it easier for you the reader to keep up to date. I will also post adjunct articles dealing with different aspects of the coronavirus, that would not necessarily fit in this article. This article covers fairly extensive number of subjects on covid. You don’t not have to read the article all at one time. Actually I would advise against it. I likewise did not write it in one sitting. One thing you will find if you have been reading my previous articles on covid, is that I am consistent in my presentation. I have never changed my opinion on how it is transmitted and how effective masks are, unlike all the supposed experts have done. You may ask why I have been able to do this? I grew up with science and medicine as bed fellows. My father groomed me for a career in medicine, He wanted me to be a doctor, but I ended up becoming an ICU nurse instead. He was somewhat disappointed, but he was still pleased and proud of my career choice. When children received comic books and Hardy Boy Books to read, I received medical books and scientific journals. So I had a bit of a strange childhood. I also had all the models of the human body and organs that were popular in the 70’s and 80’s. By the way, I tried to follow his dream for me, I did go to college and entered in a pre-med program and received a BS in Biology. Unfortunately my timing was poor and the competition was incredibly stiff for medical school positions during that period of time, and while my grades were good they did not match the 3.8 and higher GPA numbers they were looking for.
As I have stated I am not a doctor. I am not trying to prescribe any medication, make any diagnoses. Any comments I may make about treatments are my opinion only and should not be taken as recommendations. If I had covid-19 I would certainly push for them, though. I am an ICU nurse. I have been on the front lines since day one in the Coronavirus pandemic. I have also done a lot of research on the matter, since I care for these patients every day, I want to be safe. With proper precautions the Coronavirus need not be feared, but it should be respected. Whether it kills by itself or pushes people over the brink with comorbidities, it is very dangerous. I have seen many people die from it and assorted complications. This article is an attempt to dispel a lot of misconceptions on the subject and to present unbiased data, so you can make up your own mind on the matter. But if you take anything from this article please take the importance of the following; be careful, be considerate and be safe.
Coronaviruses are a family of viruses that can cause illnesses such as the common cold, severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). In 2019, a new coronavirus was identified as the cause of a disease outbreak that originated in China.
The virus is now known as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease it causes is called coronavirus disease 2019 (COVID-19). In March 2020, the World Health Organization (WHO) declared the COVID-19 outbreak a pandemic.
Public health groups, including the U.S. Centers for Disease Control and Prevention (CDC) and WHO, are monitoring the pandemic and posting updates on their websites. These groups have also issued recommendations for preventing and treating the illness.
Classification and structure:
Human Coronavirus Types
Coronaviruses are named for the crown-like spikes on their surface. There are four main sub-groupings of coronaviruses, known as alpha, beta, gamma, and delta.
Human coronaviruses were first identified in the mid-1960s. The seven coronaviruses that can infect people are:
Common human coronaviruses
- 229E (alpha coronavirus)
- NL63 (alpha coronavirus)
- OC43 (beta coronavirus)
- HKU1 (beta coronavirus)
Other human coronaviruses
- MERS-CoV (the beta coronavirus that causes Middle East Respiratory Syndrome, or MERS)
- SARS-CoV (the beta coronavirus that causes severe acute respiratory syndrome, or SARS)
- SARS-CoV-2 (the novel coronavirus that causes coronavirus disease 2019, or COVID-19)
People around the world commonly get infected with human coronaviruses 229E, NL63, OC43, and HKU1.
Sometimes coronaviruses that infect animals can evolve and make people sick and become a new human coronavirus. Three recent examples of this are 2019-nCoV, SARS-CoV, and MERS-CoV.
Covid-19 and Coronavirus is A RNA virus. This is a complicated subject and I will do my best to explain it in a meaningful manner. I have taken graduate level classes in organic chemistry, biochemistry, cell biology, immunology, microbiology, virology, genetics and molecular genetics and I still find the subject intimidating. So don’t feel bad if you have a difficult time with this subject. In order to understand viruses you need to have a basic understanding on their composition and how they reproduce. Viruses are host dependent, they cannot reproduce on their own. Reproduction is one of the requirements for true life, so in the strictest interpretation a virus is not alive. They basically are inert outside the host or in the case of Covid-19, mammals (bats, humans, dogs and even big cats, so far).
Viruses use the replication apparatus of the host cells, and have additionally developed a number of special characteristics. Scientists differentiate viruses according to the genome type – there are DNA and RNA viruses: viruses may have single-stranded or double-stranded linear RNA, single-stranded or double-stranded linear DNA, single-stranded or double-stranded circular DNA and other variations. Some viruses contain some of the enzymes required for their replication, for example the influenza virus, whose envelope not only contains an RNA genome but also an RNA polymerase. When the virus enters the host cell, the enzyme RNA polymerase starts to replicate the viral genome. The synthesis of the genome of DNA viruses usually begins at a replication origin that binds specific initiator proteins, which recruit replication enzymes of the host cell which then replicate the viral genome. RNA synthesis, like nearly all biological polymerization reactions, takes place in three stages: initiation, elongation, and termination. RNA polymerase performs multiple functions in this process: 1. It searches DNA for initiation sites, also called promoter sites or simply promoters.
In order to understand how all this works it is necessary to understand the structure of DNA and RNA.
Replication of a cell’s DNA occurs before a cell prepares to undergo division—either mitosis or meiosis I.
It takes place in three(ish) steps.
- DNA unwinds from the histones.
- An enzyme called DNA helicase opens up the helix structure on a segment of DNA, breaking the bonds between the nitrogenous bases. It does this in a zipper-like fashion, leaving a replication fork behind it.
- Here’s where things get funky.
- On the 5’–3’ strand of the DNA, an enzyme called DNA polymerase slides towards the replication fork and uses the sequence of nitrogenous bases on that strand to make a new strand of DNA complementary to it (this means that its bases pair with the ones on the old strand).
- On the 3’–5’ strand, multiple DNA polymerases match up base pairs in partial segments, moving away from the replication fork. Later, DNA ligase connects these partial strands into a new continuous segment of DNA.
Want to know something neat? When a DNA molecule replicates, each of the resulting new DNA molecules contains a strand of the original, so neither is completely “new.” Also, new histones are made at the same time the DNA replicates so that the new strands of DNA can coil around them.
Interlude: RNA vs DNA
Before we discuss transcription and translation, the two processes key to protein synthesis, we need to talk about another kind of molecule: RNA.
RNA is a lot like DNA—it’s got a sugar-phosphate backbone and contains sequences of nitrogenous bases. However, there are a couple of vital differences between RNA and DNA:
- RNA has only one nucleotide chain. It looks like only one side of the DNA ladder.
- RNA has ribose as the sugar in its backbone.
- RNA has Uracil (U) instead of thymine.
- RNA is smaller than DNA. RNA caps out at around 10,000 bases long, while DNA averages about 100 million.
- RNA can leave the nucleus. In fact, it does most of its work in the cytoplasm.
There are several different types of RNA, each with different functions, but for the purposes of this article, we’re going to focus on messenger RNA (mRNA) and transfer RNA (tRNA).
Making a Protein, Part 1: Transcription
Transcription is the first phase of the protein-making process, even though the actual protein synthesis doesn’t happen until the second phase. Essentially, what happens during transcription is that an mRNA “copies down” the instructions for making a protein from DNA.
Image from A&P 6.
First, an enzyme called RNA polymerase opens up a section of DNA and assembles a strand of mRNA by “reading” the sequence of bases on one of the strands of DNA. If there’s a C on the DNA, there will be a G on the RNA (and vice versa). If there’s a T on the DNA, there will be an A on the RNA, but if there’s an A on the DNA, there will be a U (instead of a T) on the RNA. As the RNA polymerase travels down the string of DNA, it closes the helical structure back up after it.
Before the new mRNA can go out to deliver its protein fabrication instructions, it gets “cleaned up” by enzymes. They remove segments called introns and then splice the remaining segments, called exons, together. Exons are the sequences that actually code for proteins, so they’re the ones the mRNA needs to keep. You can think of introns like padding between the exons.
Also, remember how I mentioned that a single sequence of DNA can code for multiple proteins? Alternative splicing is the reason why: before the mRNA leaves the nucleus, its exons can be spliced together in different ways.
Making a Protein, Part 2: Translation
After it’s all cleaned up and ready to go, the mRNA leaves the nucleus and goes out to fulfill its destiny: taking part in translation, the second half of protein construction.
In the cytoplasm, the mRNA must interface with tRNA with the help of a ribosome. tRNA is a type of RNA that has a place to bind to free amino acids and a special sequence of three nitrogenous bases (an anticodon) that binds to the ribosome.
Ribosomes are organelles that facilitate the meeting of tRNA and mRNA. During translation, ribosomes and tRNA follow the instructions on the mRNA and assemble amino acids into proteins.
Image from A&P 6.
Each ribosome is made up of two subunits (large and small). These come together at the start of translation. Ribosomal subunits can usually be found floating around in the cytoplasm, but a ribosome will dock on the rough endoplasmic reticulum if the protein it’s making needs to be put into a transport vesicle. Ribosomes also have three binding sites where tRNA can dock: the A site (aminoacyl, first position), the P site (peptidyl, second position) and the E site (the exit position).
Ultimately, translation has three steps: initiation, elongation, and termination.
During initiation, the strand of mRNA forms a loop, and a small ribosomal subunit (the bottom of the ribosome) hooks onto it and finds a sequence of bases that signals it to begin transcription. This is called the start codon (AUG).
Then, a tRNA with UAC anticodon pairs with this start codon and takes up the second position (P) site of the ribosome. This tRNA carries the amino acid Methionine (Met). At this point, the large ribosomal subunit gets in position as well (it’s above the mRNA and the small subunit is below).
In the elongation phase, the fully-assembled ribosome starts to slide along the mRNA. Let’s say the next sequence of bases it encounters after the start codon is GCU. A tRNA molecule with the anticodon CGA will bind to the first position (A) site of the ribosome. The amino acid it’s carrying (alanine) forms a peptide bond with Met. Afterward, the CGA tRNA (carrying the Met-Ala chain) moves to the second position and the UAC tRNA enters the E binding site. The first position site is then ready to accept a new tRNA. This process keeps going until the ribosome gets to a “stop” codon.
Termination is pretty much what it sounds like. Upon reaching the “stop” codon, the tRNA that binds to the first position carries a protein called a release factor. The amino acid chain then breaks off from the ribosome, either going off into the cytosol or into the cisterna of the rough ER, and the ribosome disassembles. However, it might very well reassemble and go around the mRNA loop again. Also, multiple ribosomes can work on the same mRNA at once!
And those are the basics of DNA!
Here’s a handy chart you can look at if you need to remember the differences between transcription, translation, and replication:
|Replication||Nucleus||Duplicate a full strand of DNA||DNA|
|2 identical strands of DNA|
|Transcription||Nucleus||Use a strand of DNA to build a molecule of mRNA||DNA|
|Translation||Cytoplasm||Use mRNA to build an amino acid chain||mRNA|
RibosometRNA (and amino acids)
|Amino acid chain (protein)|
So now yo have a better understanding of how viruses reproduce we can go to the next step, how are they are spread. So we now know that a virus is not truly a living organism and is inert until it comes in contact with a supporting host.
Modes of transmission of the COVID-19 virus
Respiratory infections can be transmitted through droplets of different sizes: when the droplet particles are >5-10 μm in diameter they are referred to as respiratory droplets, and when then are <5μm in diameter, they are referred to as droplet nuclei.1 According to current evidence, COVID-19 virus is primarily transmitted between people through respiratory droplets and contact routes. In an analysis of 75,465 COVID-19 cases in China, airborne transmission was not reported.
Droplet transmission occurs when a person is in in close contact (within 1 m) with someone who has respiratory symptoms (e.g., coughing or sneezing) and is therefore at risk of having his/her mucosae (mouth and nose) or conjunctiva (eyes) exposed to potentially infective respiratory droplets. Transmission may also occur through fomites in the immediate environment around the infected person. Therefore, transmission of the COVID-19 virus can occur by direct contact with infected people and indirect contact with surfaces in the immediate environment or with objects used on the infected person (e.g., stethoscope or thermometer).
Airborne transmission is different from droplet transmission as it refers to the presence of microbes within droplet nuclei, which are generally considered to be particles <5μm in diameter, can remain in the air for long periods of time and be transmitted to others over distances greater than 1 m.
In the context of COVID-19, airborne transmission may be possible in specific circumstances and settings in which procedures or support treatments that generate aerosols are performed; i.e., endotracheal intubation, bronchoscopy, open suctioning, administration of nebulized treatment, manual ventilation before intubation, turning the patient to the prone position, disconnecting the patient from the ventilator, non-invasive positive-pressure ventilation, tracheostomy, and cardiopulmonary resuscitation.
Based on the available evidence, including the recent publications mentioned above, WHO continues to recommend droplet and contact precautions for those people caring for COVID-19 patients. WHO continues to recommend airborne precautions for circumstances and settings in which aerosol generating procedures and support treatment are performed, according to risk assessment. These recommendations are consistent with other national and international guidelines, including those developed by the European Society of Intensive Care Medicine and Society of Critical Care Medicine and those currently used in Australia, Canada, and United Kingdom.
Precautions to take to prevent transmission:
So we know that it can be spread by droplet, suspected airborne and contact.
Lets discuss the contact part first. A recent study found that the COVID-19 coronavirus can survive up to four hours on copper, up to 24 hours on cardboard, and up to two to three days on plastic and stainless steel. Cleaning surfaces is simple and does not require expensive industrial cleaning agents. Diluted household bleach solutions can be used if appropriate for the surface. Unexpired household bleach will be effective against coronaviruses when properly diluted: Use bleach containing 5.25%–8.25% sodium hypochlorite. Do not use a bleach product if the percentage is not in this range or is not specified. Clean your hands often, either with soap and water for 20 seconds or a hand sanitizer that contains at least 60% alcohol. If you are going to continuously be in contact with contaminated surfaces wear disposable gloves. You may ask if it is airborne, why do we have to worry about surfaces? The problem is that people constantly touch there faces. If the virus is on your hands and you (don’t get grossed out, everybody does it) you pick your nose, you have now been infected.
Wearing masks: Surgical masks protect the individual from drop transmission. Since viruses are very small, you need a N95 mask to stop that form of transmission, which is called airborne. The distances vary for these transmissions, typically droplet is 3 to 6 feet, airborne particles can travel much further, so social distancing is truly problematic and anecdotal at best. All you can truly do is to lessen the risk. With both individuals wearing basic masks the risks of transmission are lessened but not eliminated. You also have to factor in length of contact. If you just have incidental contact, like say in a grocery store, the chances of having transmission are negligible. I work in the ICU. I routinely come in contact with Covid-19 positive patients for prolonged periods of time, thereby greatly increasing the risks of transmission. So I have to take care to stay healthy. If I am going to come in direct contact I wear disposable gowns. I also wear a N95 Mask and full faceshield and of course gloves. Some people wear full head gear with filtered air flow. The problem there is that multiple people wear this gear. Staff have become infected because of poor sanitizing of gear. I use my own face shield.
So if you want to guarantee total safety you can wear this mask and this shield and don’t forget gloves. But let me ask you a question, do you want to live this way?
To help prevent the spread of COVID-19, everyone should:
+Clean your hands often, either with soap and water for 20 seconds or a hand sanitizer that contains at least 60% alcohol.
+Avoid close contact with people who are sick. Put distance between yourself and other people (at least 6 feet).
+ Avoid large events and mass gatherings.
+Stay home as much as possible and keep distance between yourself and others (within about 6 feet, or 2 meters), especially if you have a higher risk of serious illness. Keep in mind some people may have COVID-19 and spread it to others, even if they don’t have symptoms or don’t know they have COVID-19.
+Stay home from work, school and public areas if you’re sick, unless you’re going to get medical care. Avoid public transportation, taxis and ride-sharing if you’re sick.
+Cover your mouth and nose with a mask when around others.
+Avoid touching your eyes, nose and mouth.
+Avoid sharing dishes, glasses, towels, bedding and other household items if you’re sick.
+Avoid sharing dishes, glasses, towels, bedding and other household items if you’re sick.
+Cover your cough or sneeze with a tissue, then throw the tissue in the trash.
+Wash your hands often with soap and water for at least 20 seconds, or use an alcohol-based hand sanitizer that contains at least 60% alcohol.
+Clean and disinfect frequently touched objects and surfaces daily.
+CDC recommends that people wear masks in public settings and when around people outside of their household, especially when other social distancing measures are difficult to maintain.
+Masks may help prevent people who have COVID-19 from spreading the virus to others. Learn more on cdc.gov
If you’re planning to travel, first check the CDC and WHO websites for updates and advice. Also look for any health advisories that may be in place where you plan to travel. You may also want to talk with your doctor if you have health conditions that make you more susceptible to respiratory infections and complications.
It has been determined that covid-19 is temperature sensitive. Temperatures of over 130 degrees kills the virus. if you believe you have been infected by covid-19, it typically resides in the sinuses for a time before it eventually gets into the blood stream. So it might be possible to eliminate the virus before you are infected by using a vics vaporizer with medicated steam. This might actually kill it, since the temperature of the steam is greater than 130 degrees and the vics might be effective as well. There are no studies being done on this as far as I know. This is me, just thinking outside the box. But what do you have to lose, right?
How It is detected?
A simple swab test of your nares and a 15 minute if you are lucky enough to have access to the rapid test.
Symptoms of covid-19:
Every virus affects the body in different ways.
Symptoms may appear 2-14 days after exposure to the virus. People with these symptoms may have COVID-19:
+Fever or chills
+CoughShortness of breath or difficulty breathing
+Fatigue Muscle or body aches
+New loss of taste or smell
+Congestion or runny nose
+Nausea or vomiting
Look for emergency warning signs for COVID-19. If someone is showing any of these signs, seek emergency medical care immediately:
+Trouble breathing or Shortness of Breath
+Persistent pain or pressure in the chest
+ Pink eye (conjunctivitis)
+Inability to wake or stay awake
+Bluish lips or face
Comorbidities that increase the lethality of the Disease:
- Serious heart diseases, such as heart failure, coronary artery disease or cardiomyopathy
- Chronic obstructive pulmonary disease (COPD)
- Type 2 diabetes
- Severe obesity
- Chronic kidney disease
- Sickle cell disease
- Weakened immune system from solid organ transplants
Other conditions may increase the risk of serious illness, such as:
- Liver disease
- Chronic lung diseases such as cystic fibrosis
- Brain and nervous system conditions
- Weakened immune system from bone marrow transplant, HIV or some medications
- Type 1 diabetes
- High blood pressure
How The Coronavirus Affects Your Body:
Complications can include:
- Pneumonia and trouble breathing
- Organ failure in several organs
- Heart problems
- A severe lung condition that causes a low amount of oxygen to go through your bloodstream to your organs (acute respiratory distress syndrome)
- Blood clots
- Acute kidney injury
- Additional viral and bacterial infections
I have included each organ or system that is affected more indepth below.
As with other coronavirusTrusted Source illnesses — including SARS, MERS, and the common cold — COVID-19 is a respiratory disease, so the lungs are usually affected first. Early symptomsTrusted Source include fever, cough, and shortness of breath. These appear as soon as 2 days, or as long as 14 days, after exposure to the virus.
While fever is at the top of the Centers for Disease Control and Prevention’s list of symptoms, not everyone who gets sick has a fever. In one study in the Journal of the American Medical Association, researchers found that around 70 percentTrusted Source of patients hospitalized with COVID-19 didn’t have a fever.
Cough is more common, but treatment guidelines developed by Boston’s Brigham and Women’s Hospital found that cough occurs in 68 to 83 percent of people who show up at the hospital with COVID-19. Only 11 to 40 percent had shortness of breath. Other less common symptoms included confusion, headache, nausea, and diarrhea.
The severity of COVID-19 varies from mild or no symptoms to severe or sometimes fatal illness. Data on more than 17,000 reported cases in China found that almost 81 percent of cases were mild. The rest were severe or critical. Older people and those with chronic medical conditions appear to have a higher riskTrusted Source for developing severe illness. This variability also shows up in how COVID-19 affects the lungs.
Some people may only have minor respiratory symptomsTrusted Source, while others develop non-life-threatening pneumonia. But there’s a subset of people who develop severe lung damage. “What we’re frequently seeing in patients who are severely ill with [COVID-19] is a condition that we call acute respiratory distress syndrome, or ARDS,” said Dr. Laura E. Evans, a member of the Society of Critical Care Medicine Leadership Council and an associate professor of pulmonary, critical care, and sleep medicine at the University of Washington Medical Center in Seattle.
ARDS doesn’t happen just with COVID-19. A number of events can trigger it, including infection, trauma, and sepsis. These cause damage to the lungs, which leads to fluid leaking from small blood vessels in the lungs. The fluid collects in the lungs’ air sacs, or alveoli. This makes it difficult for the lungs to transfer oxygen from the air to the blood.
While there’s a shortage of information on the type of damage that occurs in the lungs during COVID-19, a recent report suggests it’s similarTrusted Source to the damage caused by SARS and MERS. One recent studyTrusted Source of 138 people hospitalized for COVID-19 found that on average, people started having difficulty breathing 5 days after showing symptoms. ARDS developed on average 8 days after symptoms. Treatment for ARDS involves supplemental oxygen and mechanical ventilation, with the goal of getting more oxygen into the blood. “There isn’t a specific treatment for ARDS,” Evans said. “We just support the person through this process as best we can, allowing their bodies to heal and their immune system to address the underlying events.”
One curious thing about COVID-19 is that many patients have potentially deadly low blood oxygen levels, but they don’t seem starved of oxygen. This has led some doctors to rethink putting patients on a ventilator simply because of low oxygen levels in the blood.
The lungs are the main organs affected by COVID-19. But in serious cases, the rest of the body can also be affected. In serious cases, the rest of the body can also be affected. “In patients who become severely ill, a good proportion of those patients also develop dysfunction in other organ systems,” Evans said. However, she says this can happen with any severe infection. This damage to the organs isn’t always directly caused by the infection, but can result from the body’s response to infection.
Some people with COVID-19 have reported gastrointestinal symptomsTrusted Source, such as nausea or diarrhea, although these symptoms are much less common than problems with the lungs. While coronaviruses seem to have an easier time entering the body through the lungs, the intestines aren’t out of reach for these viruses. Earlier reports identified the viruses that cause SARS and MERS in intestinal tissue biopsies and stool samples. Two recent studies — one in the New England Journal of Medicine and a preprint on medRxiv — report that stool samples of some people with COVID-19 tested positive for the virus. However, researchers don’t know yet whether fecal transmission of this virus can occur.ADVERTISING
Evans says COVID-19 can also affect the heart and blood vessels. This may show up as irregular heart rhythms, not enough blood getting to the tissues, or blood pressure low enough that it requires medications. So far, though, it’s not clearTrusted Source that the virus directly damages the heart. In one study of hospitalized patients in Wuhan, 20 percentTrusted Source had some form of heart damage. In another, 44 percentTrusted Source of those in an intensive care unit (ICU) had an irregular heart rhythm. There are also signs that COVID-19 may cause the blood to clot more easily. It’s not clear how much this plays in the severity of the illness, but clots could increase the risk of a stroke or heart attack.CORONAVIRUS UPDATESStay on top of the COVID-19 pandemic. We’ll email you the latest developments about the novel coronavirus and Healthline’s top health news stories, daily.
When liver cells are inflamed or damaged, they can leak higher than normal amounts of enzymes into the bloodstream. Elevated liver enzymes aren’t always a sign of a serious problem, but this laboratory finding was seen in people with SARS or MERSTrusted Source. In one study of hospitalized COVID-19 patients in Wuhan, 27 percent had kidney failure. One recent reportTrusted Source found signs of liver damage in a person with COVID-19. Doctors says it’s not clear, though, if the virus or the drugs being used to treat the person caused the damage. Some people hospitalized with COVID-19 have also had acute kidney damageTrusted Source, sometimes requiring a kidney transplant. This also occurred with SARS and MERSTrusted Source. During the SARS outbreak, scientists even found the virus that causes this illness in the tubules of the kidneys.
There’s “little evidence,” though, to show that the virus directly caused the kidney injury, according to a World Health Organization report. Dr. James Cherry, a research professor of pediatrics in the David Geffen School of Medicine at UCLA, says the kidney damage may be due to other changes that happen during coronavirus infection. “When you have pneumonia, you have less oxygen circulating,” he said, “and that can damage the kidneys.”
With any infection, the body’s immune system responds by attacking the foreign virus or bacteria. While this immune response can rid the body of the infection, it can also sometimes cause collateral damage in the body. This can come in the form of an intense inflammatory response, sometimes called a “cytokine storm.” The immune cells produce cytokines to fight infection, but if too many are released, it can cause problems in the body. “A lot of [the damage in the body during COVID-19] is due to what we would call a sepsis syndrome, which is due to complex immune reactions,” Evans said. “The infection itself can generate an intense inflammatory response in the body that can affect the function of multiple organ systems.”
Another thing about the immune system is that, so far, there are almost no cases of COVID-19 in children under 9 years old. Scientists aren’t sure whether young children aren’t getting infected or their symptoms are so mild that no one notices it. Cherry says children also have a less severe illness than adults during other kinds of infections, including measles and pneumococcal infections. He says this may be because children have a “straightforward immune response,” whereas older people can sometimes have an “over-response.” It’s this excess immune response that causes some of the damage during infections. “There was evidence of this happening during SARS,” Cherry said, “and I suspect it could also be playing out here [with COVID-19].”
What has been discovered is that there are micro blood clots being formed in the body. The reason for this is not fully understood. But is suspected that this is a major causative agent for organ damage, especially the heavily vascular organs, like the kidneys and liver.
Therapeutics and treatment modalities(more will follow):
We know by now that the virus is a serious and lethal agent of infection. The more therapeutics we have on board the better. I also believe that politics and the thirst for profit should in no way be a determining factor in the selection of medications. When it comes to the lives of tens of thousands of people, the insurance companies willingness to pay should also not be a factor. I know in the past they have had a very big impact in the choice of therapeutics. We also have be willing to listen to experts from other countries when it involves the efficacy of treatments and their studies. I am sure you can see where I am going with this discussion. In order to discuss one medication in particular I have to discuss a few terms. Get your Nodoz, or caffeine this section is long.
The heart and the QT interval:
The heart is a muscular organ in most animals, which pumps blood through the blood vessels of the circulatory system. The pumped blood carries oxygen and nutrients to the body, while carrying metabolic waste such as carbon dioxide to the lungs. In humans, the heart is approximately the size of a closed fist and is located between the lungs, in the middle compartment of the chest.
In humans, other mammals, and birds, the heart is divided into four chambers: upper left and right atria and lower left and right ventricles. Commonly the right atrium and ventricle are referred together as the right heart and their left counterparts as the left heart.
The heart pumps blood with a rhythm determined by a group of pacemaking cells in the sinoatrial node. These generate a current that causes contraction of the heart, traveling through the atrioventricular node and along the conduction system of the heart. The heart receives blood low in oxygen from the systemic circulation, which enters the right atrium from the superior and inferiorvenae cavae and passes to the right ventricle. From here it is pumped into the pulmonary circulation, through the lungs where it receives oxygen and gives off carbon dioxide. Oxygenated blood then returns to the left atrium, passes through the left ventricle and is pumped out through the aorta to the systemic circulation−where the oxygen is used and metabolized to carbon dioxide. The heart beats at a resting rate close to 72 beats per minute.
The normal rhythmical heart beat, called sinus rhythm, is established by the heart’s own pacemaker, the sinoatrial node (also known as the sinus node or the SA node). Here an electrical signal is created that travels through the heart, causing the heart muscle to contract. The sinoatrial node is found in the upper part of the right atrium near to the junction with the superior vena cava. The electrical signal generated by the sinoatrial node travels through the right atrium in a radial way that is not completely understood. It travels to the left atrium via Bachmann’s bundle, such that the muscles of the left and right atria contract together. The signal then travels to the atrioventricular node. This is found at the bottom of the right atrium in the atrioventricular septum—the boundary between the right atrium and the left ventricle. The septum is part of the cardiac skeleton, tissue within the heart that the electrical signal cannot pass through, which forces the signal to pass through the atrioventricular node only. The signal then travels along the bundle of His to left and right bundle branches through to the ventricles of the heart. In the ventricles the signal is carried by specialized tissue called the Purkinje fibers which then transmit the electric charge to the heart muscle.
The normal sinus rhythm of the heart, giving the resting heart rate, is influenced by a number of factors. The cardiovascular centres in the brainstem that control the sympathetic and parasympathetic influences to the heart through the vagus nerve and sympathetic trunk. These cardiovascular centres receive input from a series of receptors including baroreceptors, sensing stretch the stretching of blood vessels and chemoreceptors, sensing the amount of oxygen and carbon dioxide in the blood and its pH. Through a series of reflexes these help regulate and sustain blood flow.
Baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Baroreceptors fire at a rate determined by how much they are stretched, which is influenced by blood pressure, level of physical activity, and the relative distribution of blood. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation. There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase heart rate. The opposite is also true. Chemoreceptors present in the carotid body or adjacent to the aorta in an aortic body respond to the blood’s oxygen, carbon dioxide levels. Low oxygen or high carbon dioxide will stimulate firing of the receptors.
Exercise and fitness levels, age, body temperature, basal metabolic rate, and even a person’s emotional state can all affect the heart rate. High levels of the hormones epinephrine, norepinephrine, and thyroid hormones can increase the heart rate. The levels of electrolytes including calcium, potassium, and sodium can also influence the speed and regularity of the heart rate; low blood oxygen, low blood pressure and dehydration may increase it.
Cardiac arrhythmias: While in the healthy heart, waves of electrical impulses originate in the sinus node before spreading to the rest of the atria, the atrioventricular node, and finally the ventricles (referred to as a normal sinus rhythm), this normal rhythm can be disrupted. Abnormal heart rhythms or arrhythmias may be asymptomatic or may cause palpitations, blackouts, or breathlessness. Some types of arrhythmia such as atrial fibrillation increase the long term risk of stroke. Some arrhythmias cause the heart to beat abnormally slowly, referred to as a bradycardia or bradyarrhythmia. This may be caused by an abnormally slow sinus node or damage within the cardiac conduction system (heart block). In other arrhythmias the heart may beat abnormally rapidly, referred to as a tachycardia or tachyarrhythmia. These arrhythmias can take many forms and can originate from different structures within the heart—some arise from the atria (e.g. atrial flutter), some from the atrioventricular node (e.g. AV nodal re-entrant tachycardia) whilst others arise from the ventricles (e.g. ventricular tachycardia). Some tachyarrhythmias are caused by scarring within the heart (e.g. some forms of ventricular tachycardia), others by an irritable focus (e.g. focal atrial tachycardia), while others are caused by additional abnormal conduction tissue that has been present since birth (e.g. Wolff-Parkinson-White syndrome). The most dangerous form of heart racing is ventricular fibrillation, in which the ventricles quiver rather than contract, and which if untreated is rapidly fatal.
Electrocardiography is the process of producing an electrocardiogram (ECG or EKG). It is a graph of voltage versus time of the electrical activity of the heart using electrodes placed on the skin. These electrodes detect the small electrical changes that are a consequence of cardiac muscle depolarization followed by repolarization during each cardiac cycle (heartbeat). Changes in the normal ECG pattern occur in numerous cardiac abnormalities, including cardiac rhythm disturbances (such as atrial fibrillation and ventricular tachycardia), inadequate coronary artery blood flow (such as myocardial ischemia and myocardial infarction), and electrolyte disturbances (such as hypokalemia and hyperkalemia).
Interpretation of the ECG is ultimately that of pattern recognition. In order to understand the patterns found, it is helpful to understand the theory of what ECGs represent. The theory is rooted in electromagnetics and boils down to the four following points:
- depolarization of the heart towards the positive electrode produces a positive deflection
- depolarization of the heart away from the positive electrode produces a negative deflection
- repolarization of the heart towards the positive electrode produces a negative deflection
- repolarization of the heart away from the positive electrode produces a positive deflection
Normal rhythm produces four entities – a P wave, a QRS complex, a T wave, and a U wave – that each have a fairly unique pattern.
- The P wave represents atrial depolarization.
- The QRS complex represents ventricular depolarization.
- The T wave represents ventricular repolarization.
- The U wave represents papillary muscle repolarization.
Changes in the structure of the heart and its surroundings (including blood composition) change the patterns of these four entities.
|P wave||The P wave represents depolarization of the atria. Atrial depolarization spreads from the SA node towards the AV node, and from the right atrium to the left atrium.||The P wave is typically upright in most leads except for aVR; an unusual P wave axis (inverted in other leads) can indicate an ectopic atrial pacemaker. If the P wave is of unusually long duration, it may represent atrial enlargement. Typically a large right atrium gives a tall, peaked P wave while a large left atrium gives a two-humped bifid P wave.||<80 ms|
|PR interval||The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. This interval reflects the time the electrical impulse takes to travel from the sinus node through the AV node.||A PR interval shorter than 120 ms suggests that the electrical impulse is bypassing the AV node, as in Wolf-Parkinson-White syndrome. A PR interval consistently longer than 200 ms diagnoses first degree atrioventricular block. The PR segment (the portion of the tracing after the P wave and before the QRS complex) is typically completely flat, but may be depressed in pericarditis.||120 to 200 ms|
|QRS complex||The QRS complex represents the rapid depolarization of the right and left ventricles. The ventricles have a large muscle mass compared to the atria, so the QRS complex usually has a much larger amplitude than the P wave.||If the QRS complex is wide (longer than 120 ms) it suggests disruption of the heart’s conduction system, such as in LBBB, RBBB, or ventricular rhythms such as ventricular tachycardia. Metabolic issues such as severe hyperkalemia, or tricyclic antidepressant overdose can also widen the QRS complex. An unusually tall QRS complex may represent left ventricular hypertrophy while a very low-amplitude QRS complex may represent a pericardial effusion or infiltrative myocardial disease.||80 to 100 ms|
|J-point||The J-point is the point at which the QRS complex finishes and the ST segment begins.||The J-point may be elevated as a normal variant. The appearance of a separate J wave or Osborn wave at the J-point is pathognomonic of hypothermia or hypercalcemia.|
|ST segment||The ST segment connects the QRS complex and the T wave; it represents the period when the ventricles are depolarized.||It is usually isoelectric, but may be depressed or elevated with myocardial infarction or ischemia. ST depression can also be caused by LVH or digoxin. ST elevation can also be caused by pericarditis, Brugada syndrome, or can be a normal variant (J-point elevation).|
|T wave||The T wave represents the repolarization of the ventricles. It is generally upright in all leads except aVR and lead V1.||Inverted T waves can be a sign of myocardial ischemia, left ventricular hypertrophy, high intracranial pressure, or metabolic abnormalities. Peaked T waves can be a sign of hyperkalemia or very early myocardial infarction.||160 ms|
|Corrected QT interval (QTc)||The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Acceptable ranges vary with heart rate, so it must be corrected to the QTc by dividing by the square root of the RR interval.||A prolonged QTc interval is a risk factor for ventricular tachyarrhythmias and sudden death. Long QT can arise as a genetic syndrome, or as a side effect of certain medications. An unusually short QTc can be seen in severe hypercalcemia.||<440 ms|
|U wave||The U wave is hypothesized to be caused by the repolarization of the interventricular septum. It normally has a low amplitude, and even more often is completely absent.||A very prominent U wave can be a sign of hypokalemia, hypercalcemia or hyperthyroidism.|
ST elevation myocardial infarctions (STEMIs) have different characteristic ECG findings based on the amount of time elapsed since the MI first occurred. The earliest sign is hyperacute T waves, peaked T waves due to local hyperkalemia in ischemic myocardium. This then progresses over a period of minutes to elevations of the ST segment by at least 1 mm. Over a period of hours, a pathologic Q wave may appear and the T wave will invert. Over a period of days the ST elevation will resolve. Pathologic Q waves generally will remain permanently.
Rhythm disturbances or arrhythmias:
- Atrial fibrillation and atrial flutter without rapid ventricular response
- Premature atrial contraction (PACs) and premature ventricular contraction (PVCs)
- Sinus arrhythmia
- Sinus bradycardia and sinus tachycardia
- Sinus pause and sinoatrial arrest
- Sick sinus syndrome: bradycardia-tachycardia syndrome
- Supraventricular tachycardia
- Atrial fibrillation with rapid ventricular response
- Atrial flutter with rapid ventricular response
- AV nodal reentrant tachycardia
- Atrioventricular reentrant tachycardia
- Junctional ectopic tachycardia
- Atrial tachycardia
- Sinoatrial nodal reentrant tachycardia
- Torsades de pointes (polymorphic ventricular tachycardia)
- Wide complex tachycardia
- Pre-excitation syndrome
- J wave (Osborn wave)
Heart block and conduction problems:
- Sinoatrial block: first, second, and third-degree
- AV node
- Right bundle
- Left bundle
- QT syndromes
- Right and left atrial abnormality
Electrolytes disturbances and intoxication:
- Digitalis intoxication
- Calcium: hypocalcemia and hypercalcemia
- Potassium: hypokalemia and hyperkalemia
Ischemia and infarction:
- Wellens’ syndrome (LAD occlusion)
- de Winter T waves (LAD occlusion) 
- ST elevation and ST depression
- High Frequency QRS changes
- Myocardial infarction (heart attack)
Now we are getting somewhere. Medications can cause a lot heart rhythm changes. The one that I want to key in on is the prolonged Q-T interval. Long QT syndrome (LQTS) is a condition in which repolarization of the heart after a heartbeat is affected. It results in an increased risk of an irregular heartbeat which can result in fainting, drowning, seizures, or sudden death. These episodes can be triggered by exercise or stress. Some rare forms of LQTS are associated with other symptoms and signs including deafness and periods of muscle weakness. Management may include avoiding strenuous exercise, getting sufficient potassium in the diet, the use of beta blockers, or an implantable cardiac defibrillator. For people with LQTS who survive cardiac arrest and remain untreated, the risk of death within 15 years is greater than 50%. With proper treatment this decreases to less than 1% over 20 years.
Many people with long QT syndrome have no signs or symptoms. When symptoms occur, they are generally caused by abnormal heart rhythms (arrhythmias), most commonly a form of ventricular tachycardia called Torsades de pointes (TdP). If the arrhythmia reverts to a normal rhythm spontaneously the affected person may experience lightheadedness (known as presyncope) or faint which may be preceded by a fluttering sensation in the chest. If the arrhythmia continues, the affected person may experience a cardiac arrest, which if untreated may lead to sudden death. Those with LQTS may also experience seizure-like activity (non-epileptic seizure) as a result of reduced blood flow to the brain during an arrhythmia. Epilepsy is also associated with certain types of long QT syndrome.
Medications that can prolong the Q-T interval:
Ok, so now that you are afraid to take any medicine, I know it is quite a list. That is why it is so important to have a doctor over see your medications and to get regular checkups, including EKG’s, especially if your medicine has cardiac side effects. But we also know is that Pharmaceutical companies like to cover the asses. So even if there is a one in the million chance that you are going to grow a third arm, they have to put it in the list of side effects. The good thing if you are told that your QT interval is lengthening, simply have the doctor change your medication or even better D/C it, and your heart will gradually return to normal. This widening effect usually occurs with prolonged use or if you are on large doses of the medication.
Did I forget to tell you that this article was going to be almost as long as War and Peace? Sorry, but we are getting close to the end, I promise. This subject is really complicated. In order to understand all the stuff these professionals are saying on TV about Covid-19, you have to have a basic understanding of a lot of stuff. Now we are ready for the therapeutic section. As I promised it will be more indepth.
I am going to start with Home treatments then move on to the hospital stuff.
At-Home Coronavirus Treatment
If your symptoms are mild enough that you can recover at home, you should:
- Rest. It can make you feel better and may speed your recovery.
- Stay home. Don’t go to work, school, or public places.
- Drink fluids. You lose more water when you’re sick. Dehydration can make symptoms worse and cause other health problems.
- Monitor. If your symptoms get worse, call your doctor right away. Don’t go to their office without calling first. They might tell you to stay home, or they may need to take extra steps to protect staff and other patients.
- Ask your doctor about over-the-counter medicines that may help, like acetaminophen to lower your fever.
- New drugs listed and recommended by Dr. William Grace: N-acetylcysteine 600mg, Vitamin-D 1000IU, Reduced glutathione 500mg, Zinc 50mg. (updated 10/21/2020 10:41PM)
The most important thing to do is to avoid infecting other people, especially those who are over 65 or who have other health problems.
- Try to stay in one place in your home. Use a separate bedroom and bathroom if you can.
- Tell others you’re sick so they keep their distance.
- Cover your coughs and sneezes with a tissue or your elbow.
- Wear a mask over your nose and mouth if you can.
- Wash regularly, especially your hands.
- Don’t share dishes, cups, eating utensils, towels, or bedding with anyone else.
- Clean and disinfect common surfaces like doorknobs, counters, and tabletops.
What to expect
Symptoms begin 2 to 14 days after you come into contact with the virus. Early studies show that many people who have mild infections recover within 2 weeks. More severe cases tend to last 3 to 6 weeks.
Therapeutics and treatment modalities Revisited:
President Trump made the mistake of mentioning a therapeutic that showed promise when the Coronavirus first burst on the scene. Hydroxychloroquine, has now become a political hot potato. It has received a lot of bad press, mainly because of biased test results. So it along with zithromax and Zinc is rarely used in the US. However it is used in the rest of the world with good results. First of all these three drugs all together cost approximately $21.00 for 5 days of treatment. That is part of the problem. Also the drug has to be given early enough to be effective, once organ damage has set in and the patient is intubated, no drug is really going to be effective. These drugs have been prescribed for decades and when taken under the guidance of a doctor have been extremely safe. But like any medicine they have to be monitored. I gave you a very scary list of medications, have these medications been banned in the US, the answer is no. They are given under strict monitoring techniques. So why has hydroxychloroquine not been given? Are we so much better than the rest of the world that we can simply ignore everybody else?
Remdesivir is another new drug on the market. While hydroxychloroquine, zithromax and zinc are recognized around the world and prescribed everywhere, Remdesevir is only licensed in the US, and is not currently authorized to be used anywhere else. Also did I forget to mention 5 days of treatment cost over $3000.00. It is so expensive that it’s use is delayed until the later stages of the disease, when the chances of it working are greatly reduced. The same holds true with convalescent Plasma, I have no idea how expensive this treatment is, but I do know that it has to be recommended by and infectious disease doctor and ordered by an intensivist. Which probably means it is also being administered too late. The only drugs cheap enough to be given immediately are being blocked in the US.
DMARDS (disease-modifying antirheumatic drugs). Clinical trials are underway to test the effect of drugs currently prescribed to suppress the immune system, in the hopes of tamping down widespread inflammation that occurs in severely ill patients. One is the biologic sarilumab (Kevzara), for patients hospitalized with COVID-19. The other biologic is tocilizumab (Actemra), for patients hospitalized with COVID-19 pneumonia. Both biologics are human monoclonal antibodies that target the immune system to decrease inflammation. (Tocilizumab is approved for treatment of cytokine storm syndrome in patients who have undergone CAR T-cell therapy for cancer.) The oral DMARD, baricitinib is in clinical trial as well.
There are other treatments and drugs on the market, but they are mainly for the treatment of the symptoms of the disease. Decadron is a steroid. It helps with the inflamation process, Lovenox and heparin are administered to reduce the occurrence of blood clots. Intravenous fluids are administered (provided they are not contraindicated) to help the patient stay hydrated and keep the kidneys flushed out.
Medical specialist have found out that patients have better outcomes if they can stay of the ventilator. Alternatively, Bilevel positive airway pressure (BiPAP) therapy, Continuous positive airway pressure (CPAP) therapy, HiFlo nasal cannulas and Non rebreather and venti masks are used. The use of ventilators is prolonged as much as possible because of the whole set of therapeutics that are usually associated with them. *
Hemodialysis and CRRT (Continuous Renal Replacement Therapy) help maintain appropriate fluid levels, and electrolytes in the blood stream, I also (and this is me thinking outside the box only) that it might be effective in reducing the blood clots in the body. I know it is an issue money. But Australia and New Zealand put over 95% of their ICU patients on CRRT, with average ICU times being around three days (pre covid numbers), thereby being cost effective in the long run.
If liver damage occurs, the use of albumin might be beneficial to shift the fluid from the tissues back into the blood stream. Advanced liver patients often have a shifting of fluid from the blood stream into the tissues. And albumin can sometimes help to reverse some of that fluid movement.
Initially patients with covid-19 were flooded with IVFs, now the trend seems to be to dry the patients out with diuretics, like lasix. Just maybe a middle of the road treatment modality might be something that should be investigated.
In mid-February, the Harvard epidemiologist Marc Lipsitch stated that this virus could infect most people in the United States if the country’s leaders did not take action. At the time, the U.S. had only a handful of confirmed cases. Few people were imagining the future Lipsitch saw—in which millions, even hundreds of millions, of Americans could fall ill. This was, at least in part, because we weren’t testing for the virus.
Lipsitch even received some criticism from scientists who felt uncomfortable with his estimate, since there were so little data to go on. Indeed, at that point, many futures were still possible. But when a virus spreads as quickly and effectively as this one was spreading in February—killing many while leaving others who had few or no symptoms to spread the disease—that virus can be expected to run its course through a population that does not take dramatic measures.
Now, based on the U.S. response since February, Lipsitch believes that we’re still likely to see the virus spread to the point of becoming endemic. That would mean it is with us indefinitely, and the current pandemic would end when we reach levels of “herd immunity,” traditionally defined as the threshold at which enough people in a group have immune protection so the virus can no longer cause huge spikes in disease.
The concept of herd immunity comes from vaccination policy, in which it’s used to calculate the number of people who need to be vaccinated in order to ensure the safety of the population. But a coronavirus vaccine is still far off, and last month, Anthony Fauci, the head of the National Institute of Allergy and Infectious Diseases, said that, because of a “general anti-science, anti-authority, anti-vaccine feeling,” the U.S. is “unlikely” to achieve herd immunity even after a vaccine is available.
In February, Lipsitch gave a very rough estimate that, absent intervention, herd immunity might happen after 40 to 70 percent of the population had been infected. The idea of hitting this level of infection implied grim forecasts about disease and death. The case-fatality rate for COVID-19 is now very roughly 1 percent overall. In the absolute simplest, linear model, if 70 percent of the world were to get infected, that would mean more than 54 million deaths.
But the effects of the coronavirus are not linear. The virus affects individuals and populations in very different ways. The case-fatality rate varies drastically between adults under 40 and the elderly. This same characteristic variability of the virus—what makes it so dangerous in early stages of outbreaks—also gives a clue as to why those outbreaks could burn out earlier than initially expected. In countries with uncontained spread of the virus, such as the U.S., exactly what the herd-immunity threshold turns out to be could make a dramatic difference in how many people fall ill and die. Without a better plan, this threshold—the percentage of people who have been infected that would constitute herd immunity—seems to have become central to our fates.
“If there is a large variability of susceptibility among humans, then herd immunity could be as low as 20 percent,” Britton told me. But there’s reason to suspect that people do not have such dramatically disparate susceptibility to the coronavirus. High degrees of variability are more common in things such as sexually transmitted infections, where a person with 100 partners a year is far more susceptible than someone celibate. Respiratory viruses tend to be more equal-opportunity invaders. “I don’t think it will happen at 20 percent,” Britton said. “Between 35 and 45 percent—I think that would be a level where spreading drops drastically.”
“This virus is proving there can be orders-of-magnitude differences in attack rates, depending on political and societal decisions, which I don’t know how to forecast.” In the context of vaccination, herd-immunity thresholds are relatively fixed and predictable. In the context of an ongoing pandemic, thinking of this threshold as some static concept can be dangerously misleading.
“COVID-19 is the first disease in modern times where the whole world has changed their behavior and disease spread has been reduced,” Britton noted. That made old models and numbers obsolete. Social distancing and other reactive measures changed the R0 value, and they will continue to do so. The virus has certain immutable properties, but there is nothing immutable about how many infections it causes in the real world.
What we seem to need is a better understanding of herd immunity in this novel context. The threshold can change based on how a virus spreads. The spread keeps on changing based on how we react to it at every stage, and the effects compound. Small preventive measures have big downstream effects. In other words, the herd in question determines its immunity. There is no mystery in how to drop the R0 to below 1 and reach an effective herd immunity: masks, social distancing, hand-washing, and everything everyone is tired of hearing about. It is already being done.
Essentially, at present, New York City might be said to be at a version of herd immunity, or at least safe equilibrium. Our case counts are very low. They have been low for weeks. Our antibody counts mean that a not-insignificant number of people are effectively removed from the chain of transmission. Many more can be effectively excluded because they’re staying isolated and distanced, wearing masks, and being hygienically vigilant. If we keep living just as we are, another big wave of disease seems unlikely.
Lipsitch stands by the February projection that Americans are likely to get the coronavirus, but not because that’s the only possible future. In other countries, it isn’t the case. “I think it no longer seems impossible that Switzerland or Germany could remain near where they are in terms of cases, meaning not very much larger outbreaks, until there’s a vaccine,” he said. They seem to have the will and systems in place to keep their economies closed enough to maintain their current equilibrium.
Other wealthy countries could hypothetically create societies that are effectively immune to further surges, where the effective herd-immunity threshold is low. Even in the U.S., it’s not too late to create a world in which you are not likely to get the coronavirus. We can wear masks and enable people to stay housed and fed without taking up dangerous work. But, judging by the decisions U.S. leaders have made so far, it seems that few places in the country will choose to live this way. Many cities and states will push backwards into an old way of life, where the herd-immunity threshold is high. Dangerous decisions will be amplified by the dynamic systems of society. People will travel and seed outbreaks in places that have worked tirelessly to contain the virus. In some cases, a single infected person will indirectly lead to hundreds or thousands of deaths.
We have the wealth in this country to care for people, and to set the herd-immunity threshold where we choose. Parts of the world are illuminating a third way forward, something in between total lock down and simply resuming the old ways of life. It happens through individual choices and collective actions, reimagining new ways of living, and having the state support and leadership to make those ways possible. For as much attention as we give to the virus, and to drugs and our immune systems, the variable in the system is us. There will only be as much chaos as we allow.
Covid-19 is nothing to mess with follow the guidelines listed by the CDC and yes even Fauci. I know he recommended face shields, which are totally impractical, unless you are caring for a loved one at home that has covid, than by all means protect yourself. A shield really does work. I would know. Good Luck and be safe.
Additional information that belongs in the conclusion section. (10/4/2020) The coronavirus that causes COVID-19 has sickened more than 16.5 million people across six continents. It is raging in countries that never contained the virus. It is resurging in many of the ones that did. If there was ever a time when this coronavirus could be contained, it has probably passed. One outcome is now looking almost certain: As much as I hate to admit it, this virus is never going away. The coronavirus is simply too widespread and too transmissible. The most likely scenario, experts say, is that the pandemic ends at some point—because enough people have been either infected or vaccinated—but the virus continues to circulate in lower levels around the globe. Cases will wax and wane over time. Outbreaks will pop up here and there. Even when a much-anticipated vaccine arrives, it is likely to only suppress but never completely eradicate the virus. (For context, consider that vaccines exist for more than a dozen human viruses but only one, smallpox, has ever been eradicated from the planet, and that took 15 years of immense global coordination.) We will probably be living with this virus for the rest of our lives.
If not, then what does the future of COVID-19 look like? That will depend, says Yonatan Grad, on the strength and duration of immunity against the virus. Grad, an infectious-disease researcher at Harvard, and his colleagues have modeled a few possible trajectories. If immunity lasts only a few months, there could be a big pandemic followed by smaller outbreaks every year. If immunity lasts closer to two years, COVID-19 could peak every other year.
At this point, how long immunity to COVID-19 will last is unclear; the virus simply hasn’t been infecting humans long enough for us to know. But related coronaviruses are reasonable points of comparison: In SARS, antibodies—which are one component of immunity—wane after two years. Antibodies to a handful of other coronaviruses that cause common colds fade in just a year.
This has implications for a vaccine, too. Rather than a onetime deal, a COVID-19 vaccine, when it arrives, could require booster shots to maintain immunity over time. You might get it every year or every other year, much like a flu shot. Even if the virus were somehow eliminated from the human population, it could keep circulating in animals—and spread to humans again. In the best-case scenario, a vaccine and better treatments blunt COVID-19’s severity, making it a much less dangerous and less disruptive disease. Over time, SARS-CoV-2 becomes just another seasonal respiratory virus, like the four other coronaviruses that cause a sizable proportion of common colds: 229E, OC43, NL63, and HKU1. These cold coronaviruses are so common that we have likely all had them at some point, maybe even multiple times. They can cause serious outbreaks, especially in the elderly, but are usually mild enough to fly under the radar. One endgame is that SARS-CoV-2 becomes the fifth coronavirus that regularly circulates among humans.
In a additional section I added that relates to Herd immunity, scientist are promulgating continuous lock downs to prevent further spread of the disease. I find this totally untenable and unsustainable. We mind as well live in the dark ages.
visiblebody.com, “DNA and RNA Basics: Replication, Transcription, and Translation,” By Laura Snider; ncbi.nlm.nih.gog, “Features, Evaluation, and Treatment of Coronavirus (COVID-19),” By, Marco Cascella; Michael Rajnik; Arturo Cuomo; Scott C. Dulebohn; Raffaela Di Napoli; healthline.com, “Here’s What Happens to the Body After Contracting the New Coronavirus,” en.wikipedia.org, “the heart,” By, wikipedia editors; webmd.com, “Coronavirus (COVID-19) Treatment,” By WebMD editors; mayoclinic.org, “Coronavirus disease 2019 (Covid-19); theatlantic.com, “The Coronavirus Is Never Going Away, No matter what happens now, the virus will continue to circulate around the world,” By Sarah Zhang; theatlantic.com, “A Vaccine Reality Check, So much hope is riding on a breakthrough, but a vaccine is only the beginning of the end,” By Sarah Zhang; theatlantic.com, “A New Understanding of Herd Immunity:The portion of the population that needs to get sick is not fixed. We can change it,” By James Hamblin;
Video showing three therapeutics in action:
This treatment modality could revolutionize the treatment for covid-19. President Trump is the first person to receive it.
*Ventilator use commonly associated medications:
+Sedation: Versed, Fentanyl, Precedex ( notable Heart rate suppression with higher doses), Propofol(should be as a last alternative, blood pressure suppression)
+Proton Pump inhibitors; Pepcid, Protonix
+Blood Pressure Support: phenylephrine, vasopressin, dopamine, levophed, dobutamine and epinephrine. All have side effects. Including shunting of blood supply to the extremities, and gastrointestinal tract. Some are hard on the blood vessels and require special large bore IV’s like PICC lines and central Lines.
+paralytics: are sometimes required to slow down the respiratory rate.
I am not a doctor, I am a nurse with a License that I have to protect. So I have to be very careful what I say, and I can’t make any recommendations, because that would be practicing medicine without a license, something I would never do. But If I had a family member in the hospital with covid I would really want an aggressive doctor. I would ask about hydroxychloroquine, zinc, zithromycin, lovenox, Remdesevir, IVF and decadron as an early treatment. And if your loved one is intubated , ask about dialysis, fentanyl and versed for sedation, no lasix unless patient is a CHF patient, heparin drip for blood clots, more decadron, and convalescent plasma, what can it hurt. Monoclonal Antibodies are coming out. Remember I am not recommending these things, just suggesting that you open up a dialog with your doctor. It pays to be a little educated on the disease and treatments when you talk to them.
Medications that are being currently tested:
Developed a decade ago, this drug failed in clinical trials against Ebola in 2014. But it was found to be generally safe in people. Research with MERS, a disease caused by a different coronavirus, showed that the drug blocked the virus from replicating. The drug is being tested in many COVID-19 clinical trials around the world. This includes studies in which remdesivir is being administered alongside other drugs, such as the anti-inflammatory drug baricitinibTrusted Source. The drug is also being tested in children with moderate to severe COVID-19.
In late April, the drug’s manufacturer, Gilead Sciences, announced one of its trials had been “terminated” due to low enrollment. Gilead officials said the results of that trial had been “inconclusive” when it was ended. A few days later, the company announced that preliminary data from another trial of remdesivir overseen by the National Institute of Allergy and Infectious Diseases (NIAID) had “met its primary endpoint.”
Dr. Anthony FauciTrusted Source, the institute’s director, told reporters the trial produced a “clear cut positive effect in diminishing time to recover.” He said people taking the drug recovered from COVID-19 in 11 days compared with 15 days for people who didn’t take remdesivir. More details will be released after the trial is peer reviewed and published. Gary Schwitzer, founder of HealthNewsReview.org, though, said the researchers changed the primary endpoint 2 weeks before Fauci’s announcement.
At the same time, another studyTrusted Source published in The Lancet reported that participants in a clinical trial who took remdesivir showed no benefits compared to people who took a placebo. Despite the conflicting results, the FDA issued an orderTrusted Source on May 1 for the emergency use of remdesivir. In early June, federal officials announced their supply of remdesivir will run out by the end of June. Gilead is ramping up production, but it’s unclear how much of the drug will be available this summer.
In mid-July, Gilead officials announced results from an ongoing phase III trial of remdesivir. They said the drug was “associated with an improvement in clinical recovery and a 62 percent reduction in the risk of mortality compared with standard of care.” They called it an an “important finding that requires confirmation in prospective clinical trials.” In mid-September, officials at Eli Lilly announced that in early stage trials their drug Olumiant when added to remdesivir can shorten hospital stays by one day for people with COVID-19. Olumiant is already used to treat rheumatoid arthritis and other conditions that involved overactive immune systems.
This antiviral was tested along with the drug lopinavir/ritonavir as a treatment for COVID-19. Researchers reported in mid-April that the two drugs didn’t improve the clinical outcomes for people hospitalized with mild to moderate cases of COVID-19.
This drug was created by scientists at a nonprofit biotech company owned by Emory University. Research in mice has shown that it can reduce replication of multiple coronaviruses, including SARS-CoV-2. Pharmaceutical company Merck and Ridgeback Biotherapeutics LP signed an agreement in May to develop this drug. It’s already being tested in a clinical trial in the United Kingdom. Unlike remdesivir, EIDD-2801 can be taken orally, which would make it available to a larger number of people.
This drug is approved in some countries outside the United States to treat influenza. Some reports from China suggest it may work as a treatment for COVID-19. These results, though, haven’t been published yet. Japan, where the medication is made, is sending the drug to 43 countries for clinical trial testing in people with mild or moderate COVID-19. Canadian researchers are testing to see whether the drug can help fight outbreaks in long-term care homes.
This is a combination of two drugs — lopinavir and ritonavir — that work against HIV. Clinical trials are being done to see whether it also works against SARS-CoV-2. One small study published May 4 in the journal Med by Cell Press found that lopinavir/ritonavir didn’t improve outcomes in people with mild or moderate COVID-19 compared to those receiving standard care. Another study, published May 7 in the New England Journal of Medicine, found that the drug combination wasn’t effective for people with severe COVID-19. But another studyTrusted Source found that people who were given lopinavir/ritonavir along with two other drugs — ribavirin and interferon beta-1b — took less time to clear the virus from their body. This study was published May 8 in The Lancet.
This drug developed by ViralClear Pharmaceuticals Inc. has been shown previously to have antiviral and immune-suppressing effects. It was tested against hepatitis C but had only modest effects. The company is running a phase II trial of this drug. People with advanced COVID-19 will be randomized to receive either merimepodib with remdesivir, or remdesivir plus a placebo. The company hopes to have results by late summer of this year.
REGN-COV2 is a combination of two monoclonal antibodies (REGN10933 and REGN10987) and was designed specifically to block infectivity of SARS-CoV-2, the virus that causes COVID-19. It appeared to help the seronegative patients, powerfully reducing the amount of virus found in nasopharyngeal swabs and alleviating symptoms more quickly. Both Lilly and Regeneron say they are discussing their data with regulators to see whether their monoclonal antibodies might warrant moving to widespread use more quickly through mechanisms like the U.S. Food and Drug Administration’s emergency use authorization process. Additional studies of their monoclonal treatments are underway in hospitalized COVID-19 patients and, separately, as preventives in uninfected people.
Biologically, a vaccine against the COVID-19 virus is unlikely to offer complete protection. Logistically, manufacturers will have to make hundreds of millions of doses while relying, perhaps, on technology never before used in vaccines and competing for basic supplies such as glass vials. Then the federal government will have to allocate doses, perhaps through a patchwork of state and local health departments with no existing infrastructure for vaccinating adults at scale. The Centers for Disease Control and Prevention, which has led vaccine distribution efforts in the past, has been strikingly absent in discussions so far—a worrying sign that the leadership failures that have characterized the American pandemic could also hamper this process. To complicate it all, 20 percent of Americans already say they will refuse to get a COVID-19 vaccine, and with another 31 percent unsure, reaching herd immunity could be that much more difficult.
The good news, because it is worth saying, is that experts think there will be a COVID-19 vaccine. The virus that causes COVID-19 does not seem to be an outlier like HIV. Scientists have gone from discovery of the virus to more than 165 candidate vaccines in record time, with 27 vaccines already in human trials. Human trials consist of at least three phases: Phase 1 for safety, Phase 2 for efficacy and dosing, and Phase 3 for efficacy in a huge group of tens of thousands of people. At least six COVID-19 vaccines are in or about to enter Phase 3 trials, which will take several more months.
We are almost five months into the pandemic and probably another five from a safe and effective vaccine—assuming the clinical trials work out perfectly. “Even when a vaccine is introduced,” says Jesse Goodman, the former chief scientist at the Food and Drug Administration, “I think we will have several months of significant infection or at least risk of infection to look forward to.”
All of this means that we may have to endure more months under the threat of the coronavirus than we have already survived. Without the measures that have beat back the virus in much of Europe and Asia, there will continue to be more outbreaks, more school closings, more loneliness, more deaths ahead. A vaccine, when it is available, will mark only the beginning of a long, slow ramp down. And how long that ramp down takes will depend on the efficacy of a vaccine, the success in delivering hundreds of millions of doses, and the willingness of people to get it at all. It is awful to contemplate the suffering still ahead. It is easier to think about the promise of a vaccine.
Vaccines are, in essence, a way to activate the immune system without disease. They can be made with weakened viruses, inactivated viruses, the proteins from a virus, a viral protein grafted onto an innocuous virus, or even just the mRNA that encodes a viral protein. Getting exposed to a vaccine is a bit like having survived the disease once, without the drawbacks. A lot remains unknown about the long-term immune response to COVID-19, but, as my colleague Derek Thompson has explained, there are good reasons to believe getting COVID-19 will protect against future infections in some way. Vaccine-induced immunity, though, tends to be weaker than immunity that arises after an infection. Vaccines are typically given as a shot straight into a muscle. Once your body recognizes the foreign invader, it mounts an immune response by, for example, producing long-lasting antibodies that circulate in the blood.
Even if all of this goes well—the earliest candidates are effective, the trials conclude quickly, the technology works—another huge task lies ahead: When vaccines are approved, 300 million doses will not be available all at once, and a system is needed to distribute limited supplies to the public. This is exactly the sort of challenge that the U.S. government has proved unprepared for in this pandemic.
Dr. Fauci Postings