Covid-19 – Spokes of the Wheel

This is a briefing on the disease covid-19: symptoms, spread, treatment, and protection against getting covid.

Covid-19

Coronavirus disease was first described in 1931, with the viruses themselves first seen in 1965, having been taken from the nasal cavities of people with the common cold and put under an electron microscope.

A “cold” is a viral disease primarily affecting the upper respiratory tract. Covid-19 is the cold caused by a virus (V2) descending from that which causes SARS (severe acute respiratory syndrome) (V1), of which China had an outbreak in 2002-2003.

V2 is over 10 times more infectious than V1 was. Conversely, covid-19 is over 10 times less lethal than SARS was.

V2 is at least 5 times as infectious as flu viruses. Peak infectiousness is typically just before symptoms show (if they ever do). Epidemiological models guess that 30-60% of V2’s spread has been via asymptomatic carriers. Asymptomatic infectiousness can last for weeks (more than 2 weeks). Children especially may be asymptomatic but infectious, though young children are typically less contagious than teens.

Roughly 40% of V2 transmissions occur asymptomatically: by people who have no covid symptoms. 35% of covid spread is by people on their 1st or 2nd day of having noticeable symptoms. By their social vivaciousness and carefree attitude, young people are playing a significant role in spreading V2.

Because V2 is so infectious, especially via silent transmission (asymptomatic contagion), a covid-19 pandemic was inevitable. V2 was spreading around the world many moons before it was discovered.

Most of those carrying V2 never develop symptoms. “Among more than 3,000 prison inmates in 4 (US) states who tested positive for the coronavirus, the figure was astronomical: 96% asymptomatic,” reported behavioral scientist Daniel Oran.

Similarly, ~95% of the covid infections in Pakistan have been asymptomatic. Pakistan’s median age is only 22 and few Pakistanis are obese.

The infectiousness of individuals varies widely. Some people are superspreaders, others not very contagious. Young children may not be as contagious as those in their early teens or older. A US study of school-age children found the infection rate among teenagers was roughly twice that of younger students. There is no way that schools can be reopened without spreading covid.

Those who are most contagious, and most likely to develop serious covid, have relatively high levels of V2 in their saliva, but not in their nasal cavity, where the samples for common swab tests are taken. Nasal mucus comes from the upper respiratory tract, whereas severe disease is associated with damage deep in the lungs. Coughing brings viral particles up to the throat, where they can pervade saliva.

Most who have develop symptoms suffer only slightly: coughing, perhaps a slight fever. Only a small percent of those infected get seriously sick. Symptoms may linger for a few weeks. Other than sudden loss of taste/smell, it is difficult to tell covid symptoms from those of the flu.

Covid is killing people at less than half the rate of seasonal flu. Covid-19 has an estimated mortality rate of only ~0.6% – though the running death rate has varied wildly in different countries owing to incomplete statistics, demographics, and the healthiness of populations. Mortality figures for infectious diseases are all statistical guesses subject to biases.

That said, more people are dying of covid-19 than typical seasonal flu because V2 is much more infectious. More people are catching covid-19, and covid-19 is more virulent to the infirm. V2 presents a Darwinist “survival of the fittest” disease to humans.

Those in poor health – including obesity, diabetes, cancer, and other chronic health conditions – are most at risk. 1/5th of those with diabetes hospitalized for covid succumb within a month. Obesity increases the risk of death from covid-19 by nearly 50% and is likely to render vaccines against V2 less effective. Being overweight is itself a disease that shortens life and invites malady. The typical report of someone who was supposedly healthy that got quite sick from covid was a fat, out-of-shape person. This is almost always the case with children who suffer from covid. 3 in 4 Americans and Brits are so overweight as to be at risk of serious covid.

Being fat is a covid liability because V2 infects fat cells. Fat serves as a ready reservoir for viral production. The fatter one is, the more territory for the virus to infect. Overweight people are also physically out-of-shape, with lamed immune systems. It’s altogether a perfect formula for covid mortality.

Severe covid sickness is not from the virus, but from misdirected immune response; hence the wide variety of complications with covid.

90% of the fatalities from covid-19 are people 60 or older, with 80% of the deaths in that age segment being people with underlying health conditions. At least 40% of all coronavirus deaths in Europe and the US have been in nursing homes.

By contrast, only 14% of covid deaths in Japan have been in eldercare facilities. 1.7% of Japanese live in nursing homes, compared to less than 1% of Americans. Japan kept elderly deaths low through hygiene and keeping the virus out. Elder care staff don’t wear face masks, which make it harder to communicate with dementia sufferers. A major difference in the severity of covid is the low incidence of obesity in Japan as contrasted to the blubbery West.

Age alone is no death sentence. Many elderly people have been infected by V2 and either had no symptoms or only modest sickness from which they recovered.

Among populations, the pattern of covid-19 deaths follow economic strata, with the poor getting sick and dying off disproportionately.

At the molecular level, the best known indicator of covid severity is the level of a specific lipid, sphingosine, and its protein precursor/producer, acid ceramidase (AC). Those with high AC and sphingosine levels are asymptomatic. Sphingosine is used on cell surfaces to protect against harmful environmental factors, including infection.

The severity of covid-19 is complex. The virulence of covid-19 varies widely, as the virus can affect lung, heart, and kidney function, and may provoke blood clotting. V2 adapted to attach to proteins on various cell types, thus increasing its versatility as well as its hazard to its host.

V2 may not be entirely flushed from the system after symptom recovery and continue to shed infectious bits post-recovery for over 2 weeks. Covid immunity in most people lasts at least 8 months. But numerous instances have been seen where covid reemerges several months after recovery. Reinfection is also possible, but “very, very rare” said American physician Ned Sharpless.

Rest and drinking plenty of fluids is about all that can be done for covid-19 – which sensibly means staying at home and lying in bed. Honey is the best medicine for covid coughs. If you have trouble breathing, lie prone rather than sitting up. Being given oxygen can help labored breathing.

Infection & Symptoms

Children, especially young ones, have much lower odds of V2 infection than adults. In adults, people with black and Asian backgrounds are at greater risk of covid infection than whites: blacks twice as likely, Asians 1.5 times more likely.

The typical entry point for V2 is inhalation though the nose. The virus finds a welcome home in the lining of the nose, because cells there are rich in a cell-surface protein (ACE2) that the virus recognizes. ACE2 normally helps regulate blood pressure. It marks tissues potentially vulnerable to infection, because the virus requires that receptor to enter a cell.

V2 does not have much chance of creating illness in healthy people, as T cells in the immune system quickly wipe it out. If the immune system doesn’t beat back the virus early, V2 marches down the windpipe to attack the lungs. The immune system causes much of the damage via inflammation and leaving a stew of fluid and dead cells that were infected. This is the underlying pathology of pneumonia and its symptoms: coughing; fever; and rapid, shallow respiration.

Ingesting V2 is another way for covid-19 to take root. V2 can attack enterocytes: the absorptive cells which line the inner surface of the small intestines.

As virologist Muge Cevik wrote, “In patients who develop severe disease, V2 elicits an aberrant host immune response.”

The immune system may zealously overreact and create a “cytokine storm,” which other viral infections are known to trigger. Cytokines are signaling molecules that guide immune response. In a cytokine storm, levels of certain cytokines soar far beyond what’s needed. Immune cells start to attack healthy tissues. Blood vessels leak, blood pressure drops, clots form, and catastrophic organ failure can ensue. “The real morbidity and mortality of this disease is probably driven by this out-of-proportion inflammatory response to the virus,” concludes American pulmonologist Jamie Garfield.

V2 reaches peak infectiousness shortly before people start to feel symptoms, and spreads like the flu. “The highest viral load is at symptom onset. Infectiousness peaks on or before symptom onset,” reported Chinese epidemiologist Eric H.Y. Lau and colleagues.

A 2021 study found that V2 contagion is highest 2 days before and 3 days after symptoms appear.

Infectiousness – what epidemiologists call reproductive ratio (R0 (pronounced “R-naught”) – is a mathematical estimation of how easily a pathogen spreads. Measles, which is incredibly infectious, has an R0 of 12 to 18.

(Note that the use of R0 as commonly used (and described here) is a technical misnomer. R_t – sometimes called R_e or “effective R” – is the moving measure of contagion. R0 is used here simply to comply with common parlance.)

The SARS virus (V1) had an R0 of 0.5, meaning that every 2 cases of SARS resulted in only 1 additional infection. The seasonal flu virus has an R0 of 1.3.

The original variant of V2 (the covid-19 virus) had an estimated peak R0 of 4.7-6.6: producing ~5-6 new cases for each initial infection. R0 is not a constant. For an epidemic to end, R0 has to drop below 1. The more recently evolved Delta variant may be 3 times more contagious.

Besides the ability for human-to-human transmission, V2 is clever enough to delay symptoms from appearing for over 2 weeks, thereby making it easier for infected victims to spread the disease. This viral savvy is termed asymptomatic infection. V2 asymptomatic covertness is how the virus has been able to be so successful in its propagation.

There is a twist to transmission by people without symptoms. People who never develop the disease covid typically have lower viral load, and so are not nearly as contagious as those who have yet to develop symptoms of covid. “These people are not the secret drivers of this pandemic,” says epidemiologist Oyungerel Byambasuren.

Infectious diseases spread in clusters. V2 is no exception, except that it, like its coronavirus cousins, seems especially prone to attacking groups of people in close proximity, especially indoors. Epidemiologists use the letter “k” to signify dispersion factor. The lower k is, the more contagion comes from a small number of people.

The flu virus responsible for the 1918 pandemic had a k of about 1 – clusters were not especially significant. SARS (V1), from which V2 descended, had a k of 0.16: quite cluster based. V2’s k is still speculative, though it’s likely near V1.

Epidemiologist Adam Kucharski thinks V2 very cluster oriented, with a k around 0.1. “Probably about 10% of cases lead to 80% of the spread,” Kucharski says. A study of Hong Kong from late January to late April 2020 found that ~19% of V2 infections seeded 80% of the spread. Spread downstream was linked to social settings such as weddings and restaurants than among people within households. Nearly 70% of the Hong Kong cases did not transmit to anyone.

As in Hong King, a study of India found covid very cluster oriented. Most new transmissions were from a few “super-spreaders”: ~10% of people causing 60% of new infections, with an average R0 of 3. Over 70% of those with covid did not transmit the virus on.

The k factor depends on people interact. Risk of infection is greatest in homes and among people of similar age. Transmission is abetted in large buildings with lots of people. Social distancing helps. Catching covid outdoors is rare indeed.

That could explain some puzzling aspects of this pandemic, including why there was such a slow pace in V2 emerging worldwide despite the virus’ infectiousness. If k is really 0.1, then most infection chains die out. Kucharski estimates that V2 needs to be introduced at least 4 times to establish itself.

That V2 is cluster oriented highlights the drawback of using R0 as a measure of contagion. R0 represents an average across a region, thereby missing outbreak variations within the region which may be considerable.

Why coronaviruses cluster so much more than other viruses is not known. Their main transmission mode – through lingering airborne mists – may be a factor.

Another likely factor in low coronavirus k seems personal. V2 k looks to be largely individual. Seriously ill or immune-compromised people shed far more virus, and for a longer duration, than others. Asymptomatic virus carriers, while somewhat infectious, shed relatively little virus.

One k factor increasingly appreciated is where clusters are most likely to form. “Clearly there is a much higher risk in enclosed spaces than outside,” says epidemiologist Christian Althaus. A Japanese study found that the risk of V2 infection is nearly 19 times higher indoors than outdoors. This explains why lockdowns seem to limit spread of this highly contagious virus.

A factor that figures against a low V2 k is its prolonged presence in those infected. V2 can shed infectious bits for weeks after symptom recovery. That’s the back-end aspect. The front end is a delayed onset of symptoms.

Those facts withstanding, typical covid-19 carriers are most infectious for only a week or so. Cluster formation therefore depends a mix of circumstances.

V2’s clustering nature can give the impression of herd immunity in the short term. Some Latin American countries, including Brazil, Europe, and China have had sudden drops in new cases – no 2nd wave – after a 1st wave of infections and social restrictions eased.

Most people don’t spread covid-19 widely. They have a low R0. The few who do – superspreaders – are in the wrong place at the wrong time. Superspreading events – which have been traced to meat processing plants, call centers, weddings and other such venues – happen when an infected person sheds volumes of virus where there are plenty of other people close by to catch it. The riskiest window for such transmission may be extremely brief — a 1- t 2-day period in the week or so after a person is infected, when viral levels are at their highest.

97.5% of people who develop symptoms from covid-19 do so within 12 days. The median incubation period for the virus is 5.1 days. There are statistical outliers. A man in Hubei China had a 38-day incubation period with no symptoms.

People are typically sick for a week from the seasonal flu. For those sickened by covid-19, it takes an average of 24 days to recover. “Reports suggest potential for clinical deterioration during the 2nd week of illness,” notes American Dr. Kathy Lofy.

Roughly 80% of those with covid-19 suffer only mild symptoms, with 15% severe and only 5% critical. Most infected may not realize it because their symptoms are so mild.

Children are only 2% of identified infections. One theory is that children have lower levels of ACE2 (angiotensin converting enzyme 2), which V2 latches onto to enter the body. “ACE2 is known to be present in our airway, kidneys, heart, and gut. There are low levels of ACE2 expression in the nasal passages of younger children, and this ACE2 level increases with age into adulthood,” explained geneticist Supinda Bunyavanich.

ACE2 is the doorknob on the outer surfaces of cells that V2 grabs onto. V2’s grip depends upon heparan sulfate, a linear polysaccharide found in all animal tissues. Protein ligands employ heparan sulfate as a tool in molecular combination for many biological processes.

Another hypothesis as to why children can neutralize the virus is that their T cells are relatively naive. T cells are part of the body’s adaptive immune system, which learns to recognize pathogens it encounters over a lifetime. Because children’s T cells are mostly untrained, they might have a greater capacity to respond to new viruses. Children’s ability to neutralize the virus might also be linked to the fact that they have a strong innate immune response from birth.

Children are also the main reservoir for seasonal coronaviruses that cause the common cold. Some researchers have suggested that antibodies for these coronaviruses might confer some protection against V2. The evidence on that hypothesis is mixed.

One hypothesis explaining why V2 doesn’t make children ill is the condition of their blood vessels. Many adults with serious covid-19 suffer blood clots. The clotting seems to be linked to malfunctioning endothelium, the smooth tissue that lines the inside of blood and lymphatic vessels and normally prevents clotting. V2 can infect endothelial cells, which are found throughout the body. Endothelium is typically in much better condition in children than adults.

If infected, covid-19 typically does not bother children much. 4% don’t show any symptoms. ~52% have mild symptoms typical of a cold. ~39% of children have moderate illness, mostly coughing. Severe cases are rare in children: only ~5% require critical care. Chinese researchers note that “young children, particularly infants, are vulnerable.” “Why most of the children’s covid-19 cases were less severe than adults’ case is puzzling,” said one the researchers, Yuanyuan Dong.

A small number of children in the US and Europe have fallen ill to Kawasaki disease or other, similar, autoimmune-provoked disease. Kawasaki disease is a rare vascular condition which is a main cause of acquired heart disease among young people. V2 can infect circulatory system cells and nervous system cells.The simplistic story is that covid-19 culls the infirm. But nothing is simple.

Researchers think V2 cannot access the womb of a pregnant woman. Researchers suspect that transmission to the fetus may be blocked not only due to the lack of virus in the mothers’ blood, but also because the major molecules used by V2 to enter cells (ACE2 receptor and TMPRSS2 enzyme) are often not physically located together in the placenta. Mother-to-fetus transfer of anti-V2 antibodies through the placenta is significantly lower than transfer of anti-influenza antibodies. 1/3rd of newborns with covid got V2 from mom during labor.

V2 can infect the brain. Its presence there may starve brain cells of oxygen.

The risk factors for getting seriously sick from covid-19 is similar to those for other respiratory illnesses. Older people and those with underlying illnesses, especially diabetes or high blood pressure, are at increased risk. Those with dementia have a much greater risk of serious covid. “Something about dementia makes you more vulnerable,” remarked American neurologist Kristine Yaffe. “Patients with cancer appear to be at increased risk of mortality and severe illness due to CoV2 infection, regardless of whether they have active cancer, are on anticancer treatment, or both,” reported a study published 28 May.

There is tremendous individual variation in how people respond – as with other diseases. Some people with known risk factors recover, and some in otherwise good health develop severe cases. The mind-body complex is an intricate gyre barely understood.

60% of all Americans have at least one chronic health condition, and 40% have more than 1. The US is a wealthy country where most people have not taken care of themselves as a lifestyle choice: through bad diet, overeating, lack of exercise, and substance abuse.

Via auto-immune response, young and middle-aged adults, barely sick with covid-19, are suffering strokes from blood clots. As an aspect of its versatility, V2 attaches to a protein common in cardiovascular cells. Immune system overreaction gums up blood flow.

Men are at greater risk and more likely to succumb to covid-19 than women. Though men and women are equally represented in infections, 64% of the reported deaths have been men. On average, older men don’t have nearly as apt an immune system response as women. In almost all animals, females are the superior sex physically and socially.

People with type A blood are more vulnerable to covid-19, whereas those with type O are more resistant. Once infected, blood type appears to have no influence on sickness or outcome.

Men have higher levels of a key enzyme that V2 latches onto than women. Whether that makes men more vulnerable to covid-19 is uncertain.

Chinese epidemiologist Gabriel Leung reports that “those most at risk of infection includes older adults, the obese and people with underlying medical conditions.”

“With respiratory infections like this, we usually see a U-shaped curve on who gets hits hardest. Young children at one end of the U because their immune systems aren’t yet developed and old people at the other end because their immune systems grow weaker,” said American virologist Vineet Menachery. “With this virus, one side of the U is just completely missing.”

“The symptoms of covid vary quite a lot from person to person, and there are a lot of symptoms that we previously didn’t appreciate were related,” reported immunologist Andrew Chan on 2 April. “As a result, there are a lot of people walking around with covid not knowing it.”

Heart problems and diabetes are especially hazardous underlying health conditions. V2 latches on to a protein found in lung and heart cells, as well as hormones which regulate blood pressure, cardiovascular and kidney function. 14-30% of covid-19 intensive care patients lose kidney function. Blood clotting is another potential problem with covid-19 which has not been seen in other coronavirus diseases.

Early symptoms of covid-19 include losing sense of smell (88%), fever (83-98%) dry cough (76-82%), fatigue (11-44%), sore throat, shortness of breath, and gastrointestinal problems (10-50%), such as diarrhea (20%). Among children, fatigue, headache and fever are the most common symptoms, with few developing a cough or losing sense of smell/taste.

Anosmia (loss of smell) switches off like a light, and takes ~7 days for recovery. V2 attacks sustentacular cells, which are in the slender sheet of tissue which lines part of the nasal cavity. These cells are thought to help maintain precise concentrations of chemicals in the nose, hence facilitating smell. 25% of those with anosmia suffer only that symptom and are otherwise asymptomatic.

Because V2 attaches to cells found in the gut as well the respiratory system, covid-19 is “almost as much a gastrointestinal illness as a respiratory illness,” says American gastroenterologist Brennan Spiegel.

“The virus can attack a lot of different parts of the body, and we don’t understand why it causes some problems for some people, different problems for others – and no problems at all for a large proportion,” pondered American neurologist Mitchell Elkind.

Children and young adults may get rashes on their toes or fingers. Viruses sometimes cause rashes – called pernio or chilblains – which are reminiscent of frostbite. These rashes may burn. The inflammation usually disappears in 2-3 weeks.

Other, less common symptoms of covid-19 include pink eye (conjunctivitis), livedo (necrosis, localized death of body tissue from lack of blood – 6%), heachaches or dizziness (36%), and a tingling, fizzing, or even burning sensation.

Those with more severe symptoms may experience a distinct pernio on the arms, legs, or buttocks. “Many of these patients also have evidence of internal clotting, such as blood clots in the veins of their legs, or in their lungs, suggesting these skin findings are a manifestation of their internal clotting tendency,” explained American dermatologist Joanna Harp.

The worst symptom of Covid-19 is pneumonia. The most effective technique for breathing with pneumonia is to lie prone, and alternate between face down and face up. It is more difficult to breathe sitting up.

Roughly 10% of infections result in symptoms 3 months after catching covid. Roughly 5% have symptoms 6 months after.

There are over 200 symptoms associated with chronic covid. Among them are mental illness (e.g., depression, anxiety), which cannot be attributed to the virus or even the physical body. As such, the classification of “long covid” is nonsensical. Treat any mention of extensive long covid among a population with skepticism.

Autoimmune attacks are typical of so-called covid “long-haulers” who have disease symptoms after the virus is gone. Reported figures vary widely, but roughly half of those who get seriously sick with covid have 1 or more persistent symptoms for months after. A study of 1,733 covid patients who were discharged from a hospital in Wuhan, China, the original epicenter of the pandemic, found that more than 75% of them still had at least 1 symptom 6 months later.

The likelihood of long covid does not correlate with severe symptoms, or even early symptoms. 1/3rd of those in California who have experienced long covid did not have any symptoms in the first 2 weeks of infection. Most of those suffering prolonged symptoms are both relatively young and overwhelmingly female, whereas those tending to be hospitalized with severe covid are mostly male and over 50.

Women are more likely to get have chronic covid than men. The most common symptoms are fatigue and mental fogginess. Long-term chronic symptoms after catching covid are an autoimmunity disease: hyperinflammatory immune response.

Treatment

Death rates from covid have dropped by over 1/4th since the pandemic began. Medical treatment has improved by greater use of steroids to jack up the bodily system, keeping patients better hydrated, and improved oxygen (supplement) therapy.

The only sensible mechanical treatment for covid-19 is providing oxygen. Being put on a ventilator is a highly invasive procedure which is seldom successful and causes numerous health complications if it is. ~88% of those put on a ventilator from covid-19 die. Those relative few who survive almost never fully recover, as the lungs are so severely damaged. “The lungs of people who have the disease for more than a month before dying is something completely different from normal pneumonia, influenza or the Sars virus. You see massive thrombosis. There is a complete disruption of the lung architecture,” reports physician Mauro Giacca.

Rather than rapidly infecting large regions of the lung, V2 sets up shop in multiple small areas of the lung. It then hijacks the lungs’ own immune cells – macrophages – and uses them to spread across the lung over a period of many days or even weeks. Macrophages typically protect the lung. V2 infects macrophages and rides them like horses to spread infection throughout the lung. As the infection slowly moves across the lung, it leaves damage in its wake and continuously fuels the fever, low blood pressure and damage to the kidneys, brain, heart and other organs that characterizes severe covid.

In early spring 2020, the US and UK ignorantly rushed to stock up on ventilators. The anticipated demand never materialized because doctors were never going to use them, knowing how seldom they are worthwhile.

Numerous anti-viral concoctions, including antibody boosters, have been tested. None have proven reliably effective. Merck’s recent molnupiravir is exemplary. Many have side effects so severe as to be as bad or even worse than covid.

Outcomes

As mentioned in the introduction, covid poses a serious health hazard for those who are not fit. Otherwise, covid is a mild cold at worst.

SARS had a mortality rate of 9.6%; 774 people died. The 1918 “Spanish flu” killed only about 2.5% of its victims, but because it infected so many people and medical care was much cruder then, 20-50 million died.

Dividing deaths by reported cases in countries with insufficient testing is inaccurate, and anyway an inapt methodology for figuring death rate. In most of the world, the number of reported cases is a tiny fraction of the total number of people infected. In other words, the denominator (# of infections) is far too small.

Methodologically, the proper calculation would be of outcomes: deaths/(recovered + dead), as active cases are unresolved. While the pandemic is ongoing, such a calculation shows a high death rate which declines as the epidemic concludes: in the instance of covid-19, in mid-September 2020 = 3% – down from over 20% in March 2020.

Antibodies have been used by vaccine makers as a metric to calibrate response to their jabs. This is convenient but simplistic accounting. Virologists Andreas Radbruch & Hyun-Dong Chang: “It is an old misconception, when advocating frequent revaccinations, that antibody concentrations during the acute immune reaction can be compared with those later on, to calculate an imaginary ‘half-life’ of antibody-mediated immunity. This ignores the biphasic character of the immune response.”

Neutralizing antibodies are 1 of 2 immediate antiviral countermeasures against coronaviruses. Such antibodies work to prevent a virus from infecting a cell. The 2nd response comes from cytotoxic T cells, which selectively eliminate infected cells.

A 3rd , later response, is the generation of helper T cell, which are specific for a virus and coordinate immune system reaction. These T cells begat immunological memory by orchestrating the emergence of long-lived plasma cells, which continue to secrete antiviral antibodies even after the virus has gone.

“People over the age of 65 are much more likely to have poor T cell responses, and a poorly coordinated immune response, and thus have much more severe or fatal covid-19,” reports infectious disease researcher Shane Crotty. “Thus, part of the massive susceptibility of the elderly to covid-19 appears to be a weak adaptive immune response, which may be because of fewer naïve T cells in the elderly.”

Immunological memory is not a long-lasting version of the immediate immune reaction to a particular virus; rather, it is a distinct aspect of the immune system. For the memory phase of an immune response, virus-specific B and T cells are maintained in a state of dormancy, but poised to revive if they encounter the virus again or a vaccine that represents it. These memory B and T cells arise from cells activated in the initial immune reaction. These cells epigenetically adapt to react rapidly to subsequent signs of infection, and drive responses geared to eliminating the disease-causing agent.

B cells have a dual role in immunity: they produce antibodies that can recognize viral proteins, and they can present parts of these proteins to specific T cells or develop into plasma cells that secrete antibodies in large quantities. Plasma cells can become memory cells themselves, and can secrete antibodies for long-lasting protection. Memory plasma cells can be maintained for decades, if not a lifetime, in the bone marrow. The presence in the bone marrow of long-lived, antibody-secreting memory plasma cells is probably the best available predictor of long-lasting immunity.

For healthy people, immunity against V2 is long-lasting. Severe covid is, after all, an autoimmune disease: provoked by the virus, but signifying an underlying unhealthiness from a damaged immune system. For those in decent health, V2 causes a mild cold at worst.

Covid-19 is endemic: a permanent member of the viral diseases to plague humanity. “This is a virus that is going to be with us forever,” says British medical scientist Mark Walport.

Spread

The global covid-19 pandemic may have begun as early as August 2019 in Wuhan, China. (Wuhan is the capital of Hubei province.) It was months later that the virus was noticed. 8 doctors warned in December of an impending outbreak and were punished for “rumor-mongering.” “Doctors in Wuhan were afraid,” said Chinese political analyst Dali Yang. “It was truly intimidation of an entire profession.”

On 14 January in a teleconference, Ma Xiaowei, head of China’s National Health Commission told health officials in Hubei province that they were facing a major challenge with covid-19. Yet China president Xi Jinping did not warn the Chinese public of covid-19 until January 20: 6 days later. By that time, over 3,000 people had been infected.

On 13 January, Chuang Yin-ching, an infectious disease specialist with the Taiwan centers for disease control, sat in a conference room in Wuhan, China, listening to local health officials describe a mysterious new virus. By the time Chuang returned to Taiwan 2 days later, he was convinced that China was hiding critical information. The next day, Chuang held a news conference to warn the world about covid-19. Though Taiwan took immediate action, the rest of the world didn’t bother to listen.

V2 was circulating in Italy by September 2019. Covid may have spread to the US as early as November 2019.

V2’s main transmission route is airborne: in virus-laden aerosols smaller than 5 micrometers in diameter. “There’s absolutely no doubt that the virus spreads in the air,” said Australian aerosol scientist Lidia Morawska. “The transmission of covid-19 is highly influenced by the airflow,” observed Chinese virologist Xiaolei Yang. “A slight change of airflow can significantly alter the virus spreading pattern.” Narrow passageways engender transmission.

V2 diffuses through the air from coughing, sneezing, and even speaking. Talking emits a small cloud of aerosols that lingers in the air for over 8 minutes. The volume of the voice indicates the thrust with which V2 is emitted.

It is entirely possible that V2 spreads through the atmosphere, as many viruses do, descending with the rain.

Viable V2 lingers in the air for many hours. In mid-January a Chinese woman had dinner with friends from Hubei province China and became infected with V2. A couple of weeks later, the woman, who had just started having covid symptoms the day before, rode on a bus to a temple ceremony in the city of Ningbo. 23 fellow bus passengers were infected during the ride. It did not matter how far a passenger sat from the infected woman on the bus. Even passengers in the very last row of the bus, 7 rows behind the infected woman, caught the virus. The bus had a cooling unit that recirculated air inside the vehicle. The outdoor ceremony in Ningbo lasted 2 1/2 hours and was followed by a brief lunch, which took place in a spacious room that did not have recirculating air-conditioning. 7 more people were infected during that time.

V2 hangs around on surfaces for as long as it can before environmental conditions degrade its integrity so badly that the virus can’t keep itself together. The virus does much better when its cool. V2 can survive on smooth surfaces for up to 28 days and on cloth 14 days. The virus may remain viable – capable of infection – for up to 24 hours on cardboard. V2 can maintain itself on human skin for 9 hours.

“Human coronaviruses can be efficiently inactivated by surface disinfection procedures with 62–71% ethanol, 0.5% hydrogen peroxide, or 0.1% sodium hypochlorite within 1 minute. Other biocidal agents such as 0.05–0.2% benzalkonium chloride or 0.02% chlorhexidine digluconate are less effective,” explains German hygienist Guenter Kampf.

Concern over fomite (surface) viral transmission is mostly misdirection, as indoor airborne transmission is by far the most common avenue of contagion. “A lot of time, energy and money is being wasted on surface disinfection and, more importantly, diverting attention and resources away from preventing airborne transmission,” said epidemiologist Kevin P. Fennelly.

Testing

The supposed key to slowing an outbreak is testing. But testing has proven uncertain. Further, no test can tell whether a person is V2 contagious.

Tests fall into 2 categories: for the V2 virus itself or for its immune system reaction. PCR (polymerase chain reaction) and antigen tests detect bits of V2.

PCR-based tests detect viral genetic molecules. As V2 lingers in the system, PCR tests return positive results long after someone stops being contagious.

China discovered that anal swab PCR testing is the most accurate by far. The drawback is its inconvenience.

Antigen tests are keyed to viral proteins, and so return positive results when a person is most infectious. Otherwise, antigen tests have been shown to be worthless. For widespread diagnostic testing, antigen tests are perhaps preferable despite their accuracy drawback and limited exposure window.

Antibody tests sense molecules that the immune system produces to remember its encounter with V2. Antibodies typically take several days to develop after an infection. As such, antibody tests have limited use for diagnosis.

Antigen assays are quick and cheap, but may result in false-negative results. Whereas PCR tests can detect a single molecule of viral RNA, an antigen test sample needs to have many thousands of viral protein bits to come up positive. PCR tests are highly accurate, but require trained personnel, specific reagents, and expensive machines that take hours to provide results. No lab is needed for antigen tests.

A common test for covid-19 is sticking a swab up the nose as far as it’ll go – a distinctly uncomfortable to downright painful procedure. One victim aptly said that it “felt like I was being stabbed in the brain.” Testing sputum (coughed up discharge) is an easier and more accurate test for V2. Testing fecal matter is also more accurate, as oral tests may return a false negative for V2 which can be revealed by testing stool.

The painful and not so good nasal torture test.

For rapid results, East Asian nations extensively used antigen tests. An infrequent problem has been patients after recovery testing positive for the virus – after they had tested negative. This resulted in uncertainty about whether V2 had cleared the system or whether a person had become reinfected – a confusion that has not been resolved.

The US is allowing all kinds of covid-19 tests which are inaccurate. The US national health safety administration has shown itself to be utterly indifferent to its responsibility.

Protection

Based on studies done in the 1930s, governmental guidelines for social distancing are commonly 2 meters. That is insufficient. A sneeze or cough outputs a cloud of droplets that may travel over 8.2 meters. “At typical indoor air velocities, a 5-micron droplet will travel tens of meters, much greater than the scale of a typical room,” says air quality maven Lidia Morawska.

Further, the virus can linger in an expelled cloud for 3 hours indoors. “The locally moist and warm atmosphere within the turbulent gas cloud allows the contained droplets to evade evaporation for much longer than occurs with isolated droplets,” explains epidemiologist Lydia Bourouiba.

To lessen the chance of catching covid-19, wash your hands after being in a public place. Do not touch your face when in a place of possible exposure. Keep your distance from others. Limit shopping to as few times a week as feasible.

“Gloves don’t really protect you because the virus sticks to the gloves the same way it sticks to your hands,” American microbiologist and infectious disease specialist Bettina Fries advises. “It’s not different.”

Masks

The first 5-8 seconds after coughing are the duration that exhaled droplets linger in the air before the cough cloud starts to disperse. Cloud volume without a mask is about 7 times larger than with a surgical mask and 23 times larger than with an N95 mask. “Anything that reduces the distance traveled by the cloud, such as a mask, handkerchief, or coughing into an elbow, should greatly reduce the region over which the droplets disperse upon coughing and therefore the chances of infection,” said physicist Rajneesh Bhardwaj.

V2 is readily airborne in nanoparticles that almost all masks don’t stop, and the virus merrily enters the eyes as well as nose and throat. Further, for those not infected, masks tend to be a source of contagion rather than a guard. Masks result in touching the face more, thus increasing the odds of catching covid-19. If a viral load is on the mask, taking it off practically guarantees viral transfer. Plastic face shields are utterly useless in containing the spread of V2 particulates. Almost everyone wears masks that afford no protection whatsoever from covid infection, though such masks may limit V2 dispersal somewhat from those contagious.

Medical masks reduce V2 aerial transmission via a cough cloud by about 60%. Cloth masks barely limit V2 aerosol dispersal. Neither type of mask protects from infection. Face shields neither protect the wearer nor stymie V2 transmission. Masks with exhalation valves allow V2 dispersal.

As a public-health policy, masks can only have any effect if their use is widespread – thereby practically requiring them being mandatory.

As a ward against contagion and a courtesy, people in East Asian nations traditionally wear masks during epidemics. Wearing masks in public to thwart covid was a passing fad in Western nations. While this was a tremendous new source of trash, mask-wearing did not make any notable difference in checking covid contagion.

References:

Ishi Nobu, “Covid vaccines,” (26 November 2020).

Ishi Nobu, “Coronaviruses & CoV2,” (17 November 2020).

Andreas Radbruch & Hyun-Dong Chang, “A long-term perspective on immunity to covid,” Nature (14 June 2021).

General references on CoV2, covid-19, and the pandemic.