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

Here is the daily world report on the covid pandemic.

Here is a link to a briefing on coronaviruses and CoV2 (V2), the virus which causes 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.

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. 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 quite overweight.

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 half 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.

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. Roughly 5% of covid-19 infections cause long-term on-off symptoms.

V2 may not be entirely flushed from the system after symptom recovery and continue to shed infectious bits post-recovery for over 2 weeks. Several instances have been seen where covid reemerges months after recovery. Reinfection is also possible, but not likely for at least 6 months.

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.

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. Rt – sometimes called Re 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.

V2 (the covid-19 virus) has 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.

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.

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 hypothesis 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 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.

V2 can access the womb of a pregnant woman. 1/3rd of newborns with covid got V2 in the womb or 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. “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.

Autoimmune attacks are typical of so-called covid “long-haulers” who have disease symptoms long after the virus is gone.

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.

In a survey of 965 South Koreans who got sick from covid, 91.1% reported that they were suffering at least one side-effect from the disease. (29 September)


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.

In early spring, 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.

Researchers discovered in mid-June that a low-cost steroid – dexamethasone – reduced deaths by 1/3rd in patients receiving mechanical ventilation, and by 1/5th in patients receiving only oxygen treatment. They found no benefit from the drug for those who did not need respiratory support.

Steroids are often used to tamp down the body’s immune system, alleviating inflammation, swelling, and pain. Many covid patients die not of viral attack, but of the body’s overreaction to the infection.

Chemically treating covid-19 has proven problematic.

On 10 July Fujifilm of Japan announced that its Avigan drug was ineffective in treating covid-19. The drug had already been approved as a covid-19 treatment in Russia and India.

A small trial in Hong Kong found that people have milder symptoms when given a combination of 3 anti-viral drugs: the anti-HIV therapy lopinavir-ritonavir, the hepatitis drug ribavirin and the multiple sclerosis treatment interferon-beta. The researchers conceded that the trial lacked the protocols used to test effectiveness or side effects. (8 May)

A large study by the World Health Organization found that remdesivir was not helpful to hospitalized covid patients. Nonetheless, the US drug regulator (FDA) has approved remdesivir for covid treatment. The US regularly approves useless, even hazardous, drugs. (23 October)

After initially claiming success by injecting covid patients with a monoclonal antibody, Eli Lily admitted 26 October that the treatment was ineffective. A monoclonal antibody is synthetic copy of an antibody produced by people who recovered from covid-19. Monoclonal antibodies are expensive to make and have high price tags: often thousands of dollars per dose. Other companies besides Eli Lily have been working on covid-19 monoclonal antibodies. Regeneron admitted 30 October that its antibody treatment was useless against severe covid. Nonetheless, the US FDA approved Eli Lily’s sham treatment for use, and the US government is buying 300,000 doses for $375 million. On 22 November, the FDA approved another worthless antibody treatment Regeneron Pharmaceuticals. (22 November)


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, on 14 September 2020 = 3% – down from over 20% in March.

How long V2 antibodies linger in the body remains controversial. 2 studies found only 2-3 months; another study indicates at least 7 months and those researchers think at least 2 years.

On average, men have a higher initial antibody response than women. But male antibody levels fall faster than females. “Men have a higher antibody response than women in the acute phase. But even though men have a higher response in the beginning, their fall in antibody levels is much quicker over time, while women seem to have more stable levels,” said virologist Samira Fafi-Kremer.

Antibodies do not convey resistance. People may have T-cell-mediated immunity without signature antibodies. Further, the antibodies discovered in many of the serological tests used are not relevant to covid immunity. The microbiome also contributes protection, though scant research has been done on this. “Public immunity to covid-19 is significantly higher than antibody tests have suggested,” says microbiologist Hans-Gustaf Ljunggren. Immunity to covid-19 may come from resistance developed from previous encounters with other coronaviruses.

Natural immunity to coronaviruses that cause the common cold might last for only a few months after infection. Even people who have high levels of antibodies against these viruses can still become infected. While immune system protection may remain, antibodies against covid-19 endure 4 months, possibly only 2-3 months in people who never develop symptoms. By contrast, antibodies from the related coronaviruses which cause SARS and MERS may linger in the system for around a year.

Antibodies are only 1 facet of effective immune response to covid-19, which typically requires a coordinated immune response. “People who mounted a broader and well-coordinated adaptive response tended to do better. A strong SARS-CoV-2 specific T cell response, in particular, was predictive of milder disease. Individuals whose immune response was less coordinated tended to have poorer outcomes,” reports infectious disease researcher Carolyn Moderbacher.

“People over the age of 65 were 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,” adds 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.”

Covid-19 is likely to be endemic: a permanent member of the viral diseases to plague humanity. “This is a virus that is going to be with us forever,” predicted British medical scientist Mark Walport. A preliminary study in China suggests that humans may never develop long-term immunity against V2, as the virus subtly mutates to evade immune systems.


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 Xo 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,” says Australian aerosol scientist Lidia Morawska.”

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.


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.

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.

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.


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.”


V2 likes the eye as an entry point – making masks a futile gesture for avoiding catching V2. 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.

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. 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 is increasingly become mandatory around the world. It hasn’t made any notable difference in checking covid contagion.

In March, the Czech Republic mandated mask wearing – the first country in Europe to do so. It was also among the first to drop that requirement in July. Facing public backlash, the Czech government has backed down from reinstating mandatory mask wearing despite a surge in new cases in early September.

Amsterdam and Rotterdam, the most populous cities in the Netherlands, no longer require face masks in many public places. Face masks are only mandatory on public transportation in the Netherlands.

Mandatory mask wearing in the US is left to state regulation. Generally speaking, American liberals have been for mandatory masks while conservatives have favored freedom over face coverings.

Swedish state epidemiologist Anders Tegnell has been a maverick on handling covid-19. Sweden did little to limit the spread of V2, insisting only on protecting the elderly and other vulnerable populations. As a result, Sweden had a severe epidemic in the spring which has since subsided. Other countries which ruined their economies with lockdowns are now having resurges and outbreaks – not really 2nd waves, as the 1st wave never quite ended. Sweden’s economy has fared better than its Nordic neighbors which implemented futile business restrictions. On masks, Tegnell said 28 July, “We see no point in wearing a face mask in Sweden. Not even on public transport.”


There are no vaccines or antivirals in routine clinical use for coronaviruses, nor for the covid-19 virus. “Their development had previously been considered as low priority because the coronaviruses that were circulating in humans caused relatively mild disease; in addition, a vaccine would need to be quadrivalent – effective against 4 different viruses – and even then would prevent only a minor proportion of colds, because the majority are caused by other viruses. As such, the development of vaccines against human coronaviruses was not pursued,” explained microbiologist Florian Krammer.

A preventative for V2 would be essentially a cure for the common cold – an incredibly lucrative prospect no drug company has been able to cash in on. “The reason why it has been so hard to develop antiviral drugs, because almost any drug that will stop viruses dead in their tracks will also stop our cells dead in their tracks,” said immunologist Shira Doron.

Traditional vaccine development takes 15 years or more.

Over 180 vaccines for V2 are now in development in numerous countries. Already over 160 potential vaccines have proven duds. Nearly 40 vaccine candidates are now at the human trial stage. This is a link to a V2 vaccine tracking website, though its explanation of vaccines is deceptive, simplistic and optimistic.

In a frenzy for vaccines, makers are publicly announcing – and touting promise – when candidates trigger immune system responses. An injected organic molecule may provoke an immune response without it having any viability whatsoever as a vaccine.

“Historically, less than 10% of vaccine candidates that go into testing are successful,” reminds Indian doctor Soumya Swaminathan, who is chief scientist of the World Health Organization.

All vaccines work on the same basic principle. A certain part or all of a pathogen is presented to the human immune system, prompting it produce antibodies which fight against infection. Traditionally, vaccines used live, weakened forms of a virus – a technique with drawbacks which can backfire.

Other vaccine techniques avoid the use of live virus at the decided risk of being ineffective or even hazardous. It’s important to remember that severe covid disease is not from the virus per se, but from inapt immune system response. “Many of the vaccine candidates have relatively strong side effects,” observed microbiologist Florian Krammer, who has studied the V2 vaccines in development. (23 October)

New genetic analysis techniques offer promise to accelerate vaccine development. But developing and testing candidates is expensive – and a risky gamble. “The reality is most vaccines will fail,” said vaccine maker Seth Berkley 4 June. And the covid-19 carrier is a novel coronavirus with considerable wiles, which means developing a vaccine for it will be an especially tricky business.

Vaccines against viral respiratory diseases are, at best, modestly effective, and only work for a short time, as viruses quickly learn how to overcome the defensive gesture. This is likely to be the case with V2, especially if antibodies are any indication – though it remains uncertain the degree to which antibodies are necessary for immunity.

Including V2, there are 5 coronaviruses in widespread circulation causing colds. “One thing we know about these coronaviruses is that people can get reinfected fairly often,” said British immunologist Stuart Neil. “The protective immunity people generate doesn’t last very long.” This has been found for covid-19 as well. “Most importantly, it puts another nail in the coffin of the dangerous concept of herd immunity,” adds British virologist Jonathan Heeney.

British vaccine developer Robin Shattock sums up the dim prospects for a V2 vaccine: “We cannot be confident natural infection will be protective for a significant proportion of individuals, nor certain of the duration of any protection. It does indicate that vaccines need to do better than natural infection. Ultimately this may require the use of annual boosting immunisations.”

Vaccines may stimulate antibodies, thus indicating to researchers a positive response. But that response may actually be wrong or ineffectual. Antibodies may not neutralize V2. Antibodies may even help V2 get into cells and replicate by causing more confusion in the immune system than identification and remedy. Some antibodies have been associated with more severe cases of covid-19. Nonetheless, antibody stimulation is the metric vaccine makers are using to deem effectiveness.

Vaccine trials typically go through 3 phases. The first 2 phases test a vaccine in small numbers of people for safety and responses, including antibody production and side effects. The 3rd phase tests thousands of people to determine efficacy: whether it lowers contagion (infection rate). This matters for achieving indirect protection in a population.

“A vaccine can provide indirect protection even if it does not fully prevent infection. Vaccines that reduce disease severity can also reduce infectiousness by reducing viral shedding and/or symptoms that increase viral spread (e.g., coughing and sneezing). A worst-case scenario is a vaccine that reduces disease while permitting viral shedding; this could fail to reduce transmission or conceivably even increase transmission if it suppressed symptoms,” wrote American epidemiologist Marc Lipsitch and American biostatician Natalie Dean. Only the Oxford-AstraZeneca vaccine trial is testing for viral load weekly regardless of symptoms. Others are not. (12 November)

A vaccine’s “efficacy” is a % reduction in disease incidence in a vaccinated group versus an unvaccinated group in a trial setting. By contrast, “effectiveness” is the ability to prevent illness among a population.

Vaccine trials are not designed, nor show, how well a vaccine may work in specific subgroups of the population. This is especially significant with covid-19, as V2 is harmless or a mild cold at worst in people in good health.

Conversely, covid presents a high risk to those with chronic health conditions, especially poorly health caused by an indulgent lifestyle, beginning with being overweight. If a V2 vaccine does not help this population subgroup, then the vaccine is practically worthless.

“A key limitation of observational studies is confounding. There may be many differences between individuals who do and do not get vaccinated, which may create noncausal correlations between vaccine status and outcomes. Such biases can threaten any observational study of vaccine effectiveness,” noted Lipsitch and Dean.

Rushing clinical trials based on antibodies is already happening. It’s a somewhat likely follow-on that vaccines will be approved on antibody production, because that’s all that can be economically be measured. Companies have been touting their vaccines based upon antibody results.

The political pressure to make any vaccine available is enormous, as is the profit potential for vaccine makers. Countries around the world are making deals with drug-makers for any vaccines that even look like they will pan out.

“The vaccines coming through fastest are the most experimental. It is possible they won’t be all that great and that others – created using more tried-and-tested but slower methods – might be better,” said British immunologist Adam Finn. “But to prove that point will become very difficult if lots of individuals have already been given the first vaccine. It will need vast numbers of people to demonstrate which is best or if a different vaccine is more suitable for particular groups, like the elderly.  If we get a vaccine that works, but not very well, it’s almost worse than not having one at all because it gets in the way of getting a better vaccine.” (25 October)

Numerous vaccine candidates are now being tested across the world. This report is not tracking each of the tests, but does announce major developments.

Britain is allowing healthy volunteers to be infected with V2 to test a vaccine candidate. “It’s a race for money and glory,” remarked microbiologist and immunologist John Moore. “That’s the reality of it.” (21 October)

China has 4 potential vaccines in phase-3 (late stage) clinical trials. 3 of those has already been approved for emergency use as part of a program to vaccinate high-risk groups. Nearly a million Chinese have gotten the vaccine by Sinopharm, a China state-owned company. (18 November)

Another vaccine from China is by Sinovac Biotech. The vaccines by Sinopharm and Sinovac are traditional inactivated virus vaccines.

Sinovac reported phase 2 trial results 17 September. The Sinovac vaccine has been shown safe so far, with by far the most common side effect lingering soreness at the injection site. The level of antibodies the Sinovac vaccine produces are less than vaccines by people who have recovered from covid, or those who have taken vaccines by Moderna or Pfizer. Whether that has any significance to effectiveness is not known.

The Sinovac vaccine is administered in 2 doses. Unlike the mRNA vaccines by Moderna and Pfizer, which need to be kept at extremely low freezing temperatures for storage, the Sinovac vaccine only needs to be refrigerated. As covid vaccines go, the Sinovac and Sinopharm vaccines look a safe bet. (20 November)

Thai virologists developed a V2 vaccine by integrating the virus’s DNA into tobacco leaves. The plant responds to the DNA and produces proteins about a week later. The vaccine has proved successful on monkeys. No follow-on report of human tests has been found by this reporter. (30 August)

China is conducting human trials on a vaccine administered through a nasal spray rather than a shot. Preliminary research indicates this technique is just as effective. (11 September)

Russia announced 12 August that the 1st batch of its barely tested “Sputnik V” vaccine will be ready by the end of August. This proved untrue. Russia is now peddling Sputnik V to other countries. To wit, on Tuesday 10 November, Russian czar Vladimir Putin declared all Russian vaccines effective. Scientists have questioned the validity of vaccine test data because multiple subjects were reported as having identical antibody levels – a “highly unlikely” outcome. To date, few Russians have been vaccinated with Sputnik 5. Russian health authorities have a history of approving medicines after limited testing, a legacy of the Soviet-era regulatory system. In a poll, 2/3s of Russians said they would not voluntarily take a Russian vaccine. Russia announced, to much skepticism, that its Sputnik V vaccine has a 95% efficacy. Russia has not released reliable data on the vaccine. Sputnik V is a 2-dose traditional vaccine that needs only near-freezing refrigeration, so is much more easily distributed than radical vaccines by Pfizer and Moderna. (24 November)

Indian drug companies have contracted to buy hundreds of million of doses of Sputnik V. India is a major consumer of Russian oil and arms. (16 September)

The covid vaccines developed in Russia and China are based on a modified form of adenovirus type five (Ad5), which “a lot of people already have immunity to” said vaccine researcher Anna Durbin. (31 August)

US drug makers Pfizer and Moderna are testing vaccines which uses messenger RNA (mRNA), a new technology that has yet to produce an approved vaccine.

Pfizer, in collaboration with German drugmaker BioNTech, announced Wednesday 18 November that analysis of its phase 3 vaccine trial of 41,135 participants suggested a vaccine that was 95% efficacious. Only 8 people got sick after getting the vaccine, out of 170 who got sick. In cases were severe covid occurred, 1 in 10 got the vaccine. The Pfizer trial data has yet to be peer reviewed. (18 November)

Because some 95% of V2 infections in healthy people only cause mild to moderate covid symptoms at worst, this shows that Pfizer’s vaccine candidate may prove worthless. (18 November)

BioNTech developed the Pfizer vaccine. There were 20 initial vaccine candidates. 5 were initially tested. Only 2 strongly provoked the immune system. The vaccine declared as successful was the one which had fewer side effects.

Ugur Sahin, chief executive of BioNTech, said 14 November that “key side effects” seen so far to its vaccine were a mild to moderate pain in the injection site for a few days, while some of the participants had a mild to moderate fever for a similar period. These side effects are worse than healthy people get from being infected with the virus. (15 November)

The messenger RNA vaccines developed by BioNTech/Pfizer and Moderna must be frozen at low temperatures prior to being administered. This freezing requirement, along with the need for 2 doses, seriously complicates vaccine distribution: putting it out of reach for some 2/3rds of the world’s nations, and problematic for any country. Between the two, Moderna has the more stable vaccine. Whereas the BioNTech/Pfizer shot must be kept between -70 °C and -80 °C from production facility to patient, Moderna’s vaccine, though normally needing to be frozen at -20 °C, may be kept at 2 °C to 8 °C for 30 days, and will last 12 hours at room temperature.

Moderna announced Monday 16 November that its phase 3 trial had shown its mRNA vaccine had a 94.5% efficacy. This percent was based on 90 patients receiving a placebo while 5 got the vaccine – a tiny number to boast such a claim. The final analysis will be of 151 covid cases among trial participants who will be followed on average for more than 2 months. Moderna’s interim test results were released by an independent data safety monitoring board. (16 November)

The 95 participants in the Moderna analysis included 15 adults aged 65 or above, and 20 participants from diverse races, including 12 identified as Hispanic, 4 African Americans, 3 Asian Americans and 1 multiracial person. Moderna said the vaccine appeared equally safe and effective in all the subgroups. (16 November)

Moderna said it had found no significant safety concerns, with most reactions being mild to moderate and short-lived. Among the reported side effects were injection site pain in 2.7% of trial volunteers after the 1st jab. After the 2nd, the most significant side effects included fatigue in 9.7%, muscle pain in 9% and joint pain in 5%. Others had headaches, other pains, or redness at the injection site. These side effects are as bad or worse for healthy people than catching covid, which has gentler viral loading than being shot twice with concentrated immune system provocation. (16 November)

At $50 to $60 US for a course of 2 shots, Moderna’s vaccine is more expensive than the other front-runners. AstraZeneca and Oxford University are aiming to sell their vaccine at $4 a dose.

US biotech firm Arcturus Therapeutics said 10 November that it expects to start distributing its messenger RNA vaccine candidate in the 1st quarter of 2021 based upon promising early stage trials. Arcturus has not released any reliable test data on its vaccine. (10 November)

Johnson & Johnson has a single-shot Ad26 vaccine that is now in phase 3 trials. J&J’s vaccine uses a cold virus to deliver V2 genetic material to spur an immune response. The platform – called AdVac – is used in a vaccine for Ebola that was approved in Europe earlier this year and has been used on more than 100,000 people, including infants, children and pregnant women. Adenovirus vaccines (such as Ad5 & Ad26) must be kept cool – making these candidates much more promising in being practical in administration to the general public. (31 October)

Johnson & Johnson plans to start testing its covid vaccine on teenagers in the US beginning in November. Pfizer has already been testing its covid vaccine candidate on teens in Germany.

With many billions of dollars at stake, competition for an accepted vaccine is fierce. Many vaccine makers are hiding data about the plans, protocols, and status of vaccine testing. Nor do these corporations state that testing data will be made available for independent review. Outside virologists are stunned about the secrecy. “Trust is in short supply,” commented Dr. Harlan Krumholz, an American cardiologist and health care researcher, on development of a covid vaccine.

While studying dengue fever, American virologist Soctt Halstead noticed in 1977 that antibodies themselves made for greater sickness upon a 2nd exposure to the disease. The effect was called antibody-dependent enhancement (ADE). ADE “is a genuine concern,” says British virologist Kevin Gilligan. “Because if the gun is jumped, and a vaccine is widely distributed that is disease enhancing, that would be worse than actually not doing any vaccination at all.” Unexpected glitches like ADE are the kind of problems vaccine developers look for in phase 3 testing of vaccines: the final testing phase that is being skipped or abbreviated in the rush for a covid-19 vaccine.

The US FDA, responsible for drug safety in that country, announced 30 August that it will approve any vaccine that doesn’t make takers drop dead, and indemnify the company that makes it to boot – especially if Trump is still president. Trump has blocked the FDA from releasing its guidelines for approving a vaccine.

The FDA is a shoddy regulator which tries to hide its activities from the public. As a matter of course, the FDA approves vaccines if the makers can show that they seem to work for at least 50% of those inoculated – which is not very effective. 1/3rd of all drugs approved by the FDA are later found harmful and recalled. (6 October)

Side effects will be a serious issue, especially considering the wide-ranging symptoms covid-19 can cause. In 1976, for instance, the “swine flu” vaccine caused an otherwise rare condition – Guillain-Barré syndrome – in which the immune system attacks the nervous system. The problem did not become obvious until the vaccine had already been injected into 45 million Americans.

The likelihood is that a V2 vaccine will be marginally effective, cause health complications in some small percentage of the people getting it, and lose what efficacy it had within a year. A cure for this cold is not going to be had in the rush that characterizes this vaccination crusade.

Another salient point is that a viable V2 vaccine will be thwarted in fat people. Obesity compromises the immune system. Therefore, a V2 vaccine won’t help those most at risk of severe covid.

“Virus biology and vaccines technology could be the limiting factors, but politics and economics are far more likely to be the barrier to immunization,” explains American public health researcher Jonathan Quick. The final hurdle is getting the vaccine to all those who need it. This is a challenge beyond sheer logistics, as plutocratic mechanics are inherent in all political institutions. Mass vaccination is a costly proposition. During the 2009 H1N1 flu pandemic, vaccine supplies were snapped up by rich nations, leaving poorer ones short.

Unsurprisingly, a small group of wealthy countries has bought more than half of the expected supply of the most promising vaccines. Nearly 2/3rds of the world’s population would not have a vaccine until at least 2022. (17 September)

In an alliance led by the World Health Organization, 156 countries have joined a global scheme intended to ensure fair distribution of vaccines against covid-19. The US has not. (21 September)


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

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