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July 2020

Even More Good News On The Vaccine Front

The NIH just announced that a Phase 3 clinical trial of a CoV-2 RNA vaccine was launched today. The highly novel vaccine, developed by the National Institute of Allergy and Infectious Diseases and the biotech company, Moderna, uses no virus vehicle, just a segment of the CoV-2 RNA genome. This is a highly novel approach since no RNA vaccine has been developed to any pathogen. If successful, it will revolutionize vaccinology by eliminating any infectious vehicle that could cause side effects. It also will dramatically speed novel vaccine development since all you need is a genetic sequence of the pathogen, after which it is simple to produce in any lab. It is the second RNA vaccine under development that will soon enter phase 3 testing. The other vaccine is being developed by the pharma giant Pfizer and the German biotech company, BioNTech, and is expected to also enter phase 3 trials in a few days.

Since about 30,000 volunteers are needed for this trial, it is being conducted at 89 partner sites around the US, under the oversight of the The NIH Coronavirus Prevention Network (CoVPN). Adults who are interested in joining this study can visit www.coronaviruspreventionnetwork.org(link is external) or visit ClinicalTrials.gov and search identifier NCT04470427 to find a study center to volunteer.

Seeing how the virus continues to spread in most states, even accelerating its spread in many states, makes it increasingly possible that an effective vaccine will be available by the end of the year. Even if that happens, we will still need more time to understand other variables, such as how long the immunity lasts, and how well people over 60 are protected.


New Insight To CoV-2 Function Leads To New Drug Candidates

Two ways to infect cells: An elegant study recently published in the journal Cell, reports that when the SARS-CoV-2 virus infects a human cell, it causes the cells to sprout appendages studded with viral particles. These disfigured cells appear use those appendages, or filopodia, to reach still-healthy neighboring cells. The protuberances then bore into the adjacent cells’ bodies and inject their viral venom creating a newly infected neighbor.

8c88fa7db69ff0e7b932642a5114a145Image shows filopodia and viral buds in a CoV-2 infected cells. An uninfected cell would be much smoother and not show the appendages or buds. The Electron micrograph was taken by Dr. Elizabeth Fischer at the National Institute of Allergy and Infectious Disease Rocky Mountain Laboratory.

Until now, it was assumed that the process by which the coronavirus spreads in a body was pretty standard: It binds to receptors on cells that line humans’ mouth, nose, respiratory tract, gut, lungs and blood vessels. Then it docks to the receptor and the cell engulfs it. It then takes over cellular machinery to produce new viruses that bud out of the cell and enter the host’s circulation in search of a new target cell, perhaps far from the cell from which it budded. While effective, this mechanism of viral spread also exposes the free-floating viruses to the host’s immune defenses. Hence, the close-quarters attack mediated by viral-studded filopodia provides a second, more secure way for the virus to spread. It enhances the efficiency of establishing an infection.

While this is a new finding for CoV-2, other viruses are also known to use the filopodia infection mechanism. Vaccinia virus, which causes smallpox, HIV, and some flu viruses use filopodia to enhance their ability to break-and-enter into cells. But these viruses do not seem to set off the prolific growth of filaments to the extent that was observed on coronavirus-infected cells.

Practical benefits of the research finding: The research emerges from an ambitious effort to identify potential COVID-19 treatments using “quantitative biology,” and “proteomics” to identify global changes in protein expression and function that are affected by infection with the virus. This can provide a snapshot of how cellular biochemical pathways and processes are rewired upon infection. This is in silico, or computer-based, research that mines vast databases on protein structure, protein function, protein interaction, and chemical (drug) interference to find chemicals that can inhibit CoV-2 activity. These databases were generated over the last two-to-three decades and still grow rapidly. 

UC San Francisco scientists examined global changes in cell protein expression and function and found wide ranging effects of CoV-2 infection in cells, including a shutdown of proteins that drive cell growth, and activation of an enzyme that causes changes in the cytoskeleton and promotes filopodia production. They, and their collaborators, then mined information from the databases that led them to several compounds known to interfere with the biochemical changes caused by the virus.

With this in silico research, the investigators identified several potential drugs that could disrupt the chemical signals that activate filopodia production, thereby possibly crippling this mechanism of viral spread. Several of the compounds showed ability to inhibit virus production in tissue culture experiments. Among the seven drugs they identified as potentially useful against the virus are Silmitasertib, an experimental drug in early clinical trials as a treatment for bile duct cancer and a form of childhood brain cancer; ralimetinib, a cancer drug developed by Eli Lilly; and gilteritinib (marketed as Xospata), a drug in use already to treat acute myeloid leukemia.

This is how drug discovery is done now days.

The research was a collaboration between scientists from UC San Francisco, Mt. Sinai in New York City, the NIH Rocky Mountain Labs in Montana, the Pasteur Institute in Paris and the University of Freiburg in Germany.


Good Progress On The Vaccine Front

At last tally 197 vaccine candidates against the CoV-2 virus are being developed around the world. On May 12, that number was 125. It seems that vaccine candidates are spreading as fast as the virus. According to the World Health Organization, 23 of these experimental vaccines already are in human trials. As reported two months ago in these pages, the vaccine that seems to have the early lead is being developed at England’s Oxford University in partnership with the pharma company AstraZeneca. On Monday, they reported encouraging results from their combination phase 1/2 study in the journal The Lancet.

Jenner instThe Jenner Institute, Oxford University

It also seems that two other vax candidates have caught up to the Oxford efforts and also have reported encouraging results in early combination phase 1/2 or phase 2 studies. One of the vaccines is being developed by the Chinese company CanSino Biologics, which also published its results from early phase 2 trials on 500 subjects in the same issue of The Lancet. Both the Oxford and Chinese labs are developing a recombinant vaccine in which the genetic sequence for the CoV-2 spike protein is engineered to be expressed as part of a crippled adenovirus genome. The adenovirus will infect human cells, but not replicate or cause disease. 

The third vaccine is being developed by the pharma giant Pfizer and the German biotech company, BioNTech. This is a highly novel RNA vaccine where just a simple genetic sequence from the CoV-2 virus is used to immunize patients. No virus is used at all, just some of the virus genetic material. They recently reported in a pre-print paper that has not yet been peer-reviewed, similarly encouraging results from a combination phase 1/2 trial on 60 subjects.

The results of the three studies were very similar. The vaccines were all safe and there were no serious side effects. The only problems were an occasional temporary fatigue, sore arm or headache, which were treated with Tylenol. These effects are much more pleasant than coming down with COVID-19.

Importantly, all three vaccines were shown to stimulate both arms of the adaptive immune response, which is a crucial factor for a successful vaccine. The first arm is the B cell, or bone marrow-derived lymphocyte response. B cells produce antibodies that neutralize the virus, but they fade away after the infection is cleared, not providing long term immunity. The second arm is the thymus-derived lymphocyte, or T cell, response. Activating a T cell response is particularly important for a successful vaccine because it is what oversees the whole immune response to a pathogen and, more importantly, produces long lived memory T cells that impart a long term sentry function to the pathogen, which is what “immunity” is. Memory cells are the basis for long-lived vaccine protection. A successful vaccination will produce memory cells that will sound an alarm if you are later exposed to the pathogen. This alarm rapidly mobilizes your immune system to make a very robust defense that prevents the infection from developing. Therefore, it is very encouraging that the experimental vaccines activated T cell responses.

The Oxford vaccine stimulated T cell immune responses within 14 days and antibody responses in 28 days. Both responses were also stimulated within 28 days in the Chinese study. The Oxford and Chinese studies showed that 85-90% of vaccinated subjects developed antibodies that neutralized the virus and that response was sustained up to 56 days, which is how long the longest study followed the recipients. T cell responses were also seen in 90-100% of the vaccine recipients. The Chinese study further reported that people over 55 developed weaker responses than younger subjects, which was expected. The Oxford study only enrolled volunteers under 55 years. While employing a much smaller sample size, the German study had results similar to the Oxford and Chinese studies.

It must be cautioned that these very encouraging phase 1 and 2 studies did not test whether the immune response could actually protect people from the virus. In other words, they did not test whether the vaccines produced memory cells that could confer long-term immunity. This will be tested in the large phase 3 trials that will begin as early as the end of July. These will be massive studies involving tens-of-thousands volunteers. Phase 3 studies also will take longer since they require the subjects to be naturally exposed to the virus and develop COVID-19. After a period of time, the number of unvaccinated control subjects who develop the disease will be compared to the COVID-19 incidence in vaccinated subjects in order to learn if, and to what extent, the vaccine can protect against the virus. These results should be forthcoming in a few months. Phase 3 trials also will pay attention to vaccine safety in a much larger cohort of subjects than tested in the earlier trials.

If the phase 3 studies show that the vaccines can protect people against future infection with the virus and are safe, then they will be approved. In anticipation of this, some large pharma companies, such as AstraZeneca and Pfizer are already producing the, still experimental, vaccines. This means that if they prove effective, there will be a stockpile of vaccine that can be immediately dispensed around the world. The companies also have pledged to provide the vaccines at cost.

Just a few weeks ago, worry was that the virus seemed to be petering out and that it would be hard to find sufficient numbers of volunteers to undertake large phase 3 studies. However, as the virus is rebounding in most US States and is gathering steam elsewhere in the world, that does not seem to be a problem anymore. Just one week after the National Institutes of Health launched a clinical trial network for vaccines and other prevention tools to fight the pandemic, they announced that 107,000 Americans have already volunteered for vax studies. It is estimated that 120,000 volunteers are needed to adequately test the four lead vaccine candidates under development in the US (assuming 30,000 subjects are needed to test each vaccine). So the high enrollment is a good sign that the vax studies will not be hampered by low enrollment.

Stay tuned. We will see.


Using And Re-Using N95 Face Masks

In these pages, I previously talked about the basics of face masks, and how their wide spread use might have the same, if temporary, effect of attaining herd immunity. Keep in mind that your typical cloth mask or bandana mostly protects others from oral spray from an infected wearer. They are not very effective at protecting the wearer since most of the inhaled air comes in from the edges and is not well filtered by the mask. In order to protect yourself from airborne virus, you need to wear an N95 respirator mask that is fitted to your face. Early on, the masks were hard to find, but, lately I have seen long shelves of them at hardware stores.

Peter Tsai is the Taiwanese/American who invented the synthetic fabric that make N95 masks effective at filtering 95% of particles in the air. Tsai made the fabric using an electrostatic charging method. Put simply, the mask's filter contains both positive and negative charges. Neutral particles, like bacteria and viruses, gain a charge when they contact the fabric, trapping them before they can pass through the mask.

Tsai was retired for two years when the pandemic struck. Because of the early shortage of N95 masks, he heard that healthcare workers were reusing them, so he went back to work at the University of Tennessee, Knoxville’s Research Foundation to research the best way to sterilize the masks for re-use. He tested a variety of methods: He left the masks out in the sun, put them in the oven, washed them with soap and steamed them. The best method, he found, was keeping the masks in 160-degree dry heat for 30 minutes, which can be done by hanging them in an oven.

But that's not his preferred method. Tsai recommends buying seven N95 masks and rotating them, using a new one each day. After using one mask, he hangs it in an isolated spot and doesn't use it again for seven days, so any pathogen it catches becomes inactive over time. Various environmental studies of the CoV-2 virus find that it survives a few hours to a few days, depending on the surface the virus is on. It seems to have a shorter survival time on cloth and fabric, perhaps due to desiccation of the virus particles caused by the absorptive properties of the material.

While wearing N95 masks will greatly reduce respiratory exposure to the virus, they are not perfect. You can still pick it up from surfaces and you can even be infected by airborne virus through your eyes. Also, the masks can be quite uncomfortable, and if worn for hours at a time, cause bruising and skin irritation where it fits to the face as shown in the selfie below. Also, be aware that extended use of the respirators can lead to reduced oxygen levels in the blood. One report a few weeks ago told of a nurse who passed out after wearing her mask for several hours. Therefore, only wear them when you are in a crowded situation or in a room, like an elevator that has been recently occupied by many people where virus could remain in the air. Do not wear them in your home, car or outside when you are well separated from others.

Finally, remember these recommendations apply only to the N95 respirator masks. They do not apply to regular masks that are not very effective at protecting the wearer. They are much better at protecting others from an infected wearer.

Bruising


Misleading Media Reports That CoV-2 Immunity Quickly Disappears

The media is reporting that immunity to CoV-2 disappears in a few months. This is based on a pre-publication report from researchers at King’s College in London that shows that of >90 infected patients, only 17% maintained significant levels of anti-CoV-2 antibodies after three months. The antibody response to the virus decays pretty quickly after the virus is cleared from an infected person’s body. The implication is that we quickly lose immunity to the virus.

However, this is a good example of how poorly the media sometimes reports on medical science matters.

In every infection that generates antibodies, the antibody level always decays pretty quickly after the infection runs its course. And thank goodness for that because your blood serum could be overloaded with protein if you kept pumping out antibodies to everything you were ever exposed to. Most readers of this blog have had numerous vaccinations in their youth and remain immune to most of the pathogens they were vaccinated against or exposed to. You don’t keep producing antibodies to all those pathogens throughout your life, but you still remain immune to those pathogens. How does that happen?

Antibodies are just one arm of your immune response to an infection. Antibodies are produced by blood cells called lymphocytes, specifically bone marrow derived lymphocytes, or B cells. When you are first infected with a pathogen, it takes some time for the B cells to be informed that there is an invader, but they gradually begin producing antibodies to that bug. Once the bug is eliminated, the B cells cool off and go into a dormant mode.

There also is another type of lymphocyte called T cells because they originate in the thymus, a gland in your neck. They come in different forms. There are cytotoxic T cells which recognize virally infected cells and kill them. There also are T cells, called helper cells, that encourage B cells and cytotoxic T cells to attack the invader. All of these go dormant after the infection is over. However, a type of T cell, called a memory cell, arises during the infection and floats in your blood as a sentinel guarding, often for many years, against future infection.

Memory cells, not antibodies are the basis of vaccination and immunity. If you are subsequently exposed to the same pathogen, memory cells sound an alarm that immediately mobilizes your dormant B cells and cytotoxic T cells to provide a quick response to an infection with a previously experienced pathogen.

 So, the media articles implying that immunity to CoV-2 is short lived because the antibody response decays after three months are misleading. The fact of antibody decay does not mean that you are losing immunity. You are also developing memory cells while the B cells that produce antibodies are going into sleep mode.


Texas Replaces NYC As The New Hotspot

A 30-year old man who attended a COVID party in San Antonio has died from the disease. Before he died, he told doctors that he thought the virus was a hoax and intended to prove it with the party. He reportedly concluded, “I made a mistake.” Bexar County, where San Antonio is has about 19-20,000 confirmed COVID cases and is seeing about 1000 new cases a day. Most cases are in people aged 20-39.

Elsewhere, in Harris County Texas, Houston hospitals are full and ICUs are overwhelmed requiring COVID patients to wait in ERs for a bed. Because of this, Houston hospitals are also increasingly diverting ambulances to other regional hospitals, which also affects non-COVID patients, such as those with cardiovascular emergencies. There has been a spike in at-home deaths from cardiac arrest in the county, which could be directly from COVID disease or from delayed medical attention to non-COVID patients.

During an eight-day period in late June and early July, Houston’s 12 busiest emergency departments hit a maximum capacity three times, in contrast to zero times in the same period a year earlier. And when a hospital does have beds available, they sometimes do not have the staff to manage those patients, due to COVID-related absences.

On June 24, several hospital executives affiliated with the Texas Medical Center — a sprawling medical campus that’s home to most of Houston’s major hospital systems — issued a warning that COVID-19 hospitalizations were growing at an “alarming rate” and could soon put an unsustainable strain on hospital resources. They were right.

The mortality rate from COVID is decreasing, but the number of people getting very ill is increasing. That is likely because the virus is running rampant in younger people who flaunt social isolation. What they don’t realize is that many infected young people will have long lasting health problems as previously reported in these pages.

It is noteworthy that Texas was one of the first states to open back up.


‘Superspreading’ Drives Most COVID-19 Spread

  • On March 10, a choir practice in Skagit County Washington was attended by 61 people, including one who had developed a “cold” three days prior to the practice. In the days following the 2.5 hour practice, 52 COVID-19 cases occurred (an infection rate of 87%). Three were hospitalized and two died from the disease.
  • A couple of weeks before that choir practice, a Boston biotechnology company held a two-day leadership conference for about 175 of its world-wide executives. Apparently, someone was unknowingly infected and it spread to participants who took it back to their homes. At least 99 people from the meeting alone came down with COVID-19.
  • About the same time, a funeral in Albany, GA was attended by >100 people. The virus was in attendance as well leading to a huge outbreak that spread into surrounding rural areas causing one of the nation’s largest local outbreaks of COVID-19.
  • In Arkansas, an infected pastor passed the virus to more than 30 Sunday church attendees, three of whom died.

Epidemiology:

Somewhere between 10-20% of infected people are likely responsible for 80% of COVID-19 cases as recently described in Scientific American and reported in a study published in the Proceedings of the National Academy of Sciences. These “superspreaders” are typically asymptomatic and under the age of 60 according to investigators at Emory University’s Rollins School of Public Health.

Epidemiologists who study infectious diseases refer to the R0, or “R naught,” value, which is a mathematical description of the reproduction number of an infectious disease. Seasonal flu has an R0 of about 2, meaning that each infected person, on average, will spread the virus to two more people. The R0 for Cov-2 is about 4, meaning it is twice as infectious as the flu. For comparison, the R0 for measles, the most infectious virus we know, is 12-18. For the SARS pandemic in 2003, the early R0 was about 2.75 but soon was brought down to <1 due to isolation strategies.

In addition to R0, scientists use a value called the dispersion factor (k), which describes how much a disease clusters. The lower k is, the more the transmission clusters, or comes from a small number of people. A 2005 Nature paper estimated that SARS had a k of 0.16. The estimated k for MERS, which emerged in 2012, is about 0.25. In the Spanish flu pandemic of 1918, in contrast, the value was about one, indicating that clusters played much less of a role in spreading the Spanish flu than it did in spreading the SARS and MERS coronaviruses.

Current estimates of k for CoV-2 vary. In January, researchers at the University of Bern concluded that k for COVID-19 is somewhat higher than for SARS and MERS. In a recent preprint, it was estimated that k for COVID-19 is as low as 0.1, which means that probably about 10% of cases lead to 80% of the spread.

Superspreading:

According to the CDC, super spreading is caused, in part, by individuals known as “superemitters,” who release more aerosol particles during speech than do their peers. Some people shed far more virus, and for a longer period of time, than others, perhaps because of differences in their immune system or the distribution of virus receptors and virus in their body.

Yet, other factors play a role in creating superspreader events. These are physical factors including crowd size, close contact, closed environment, and ventilation. Japanese researchers found that CoV-2 transmission was 18 times greater in a closed vs open-air space. Unsurprisingly, London researchers also found that the largest clusters of outbreaks were in indoor spaces like nursing homes, churches, schools, shopping areas, dormitories, prisons and ships.

It makes sense that an important factor in creating a superspreader event is the number of people involved. If a group of five friends meet, the chance of a superspreader event is much less than if 500 met. Plus, the chance of having an infectious person in the group is much reduced in the group of five vs 500. Hence, it makes sense to limit the size of gatherings in attempt to limit superspreader events.

Time also plays a key role in the virus spread. Various groups consider 10-15 minutes contact with an infected person to be the magic limit. This might help explain why grocery store cashiers, who only interact with customers for a couple of minutes, have not been hard hit with the virus, while meat-packing employees who work long shifts side-by-side, have been hard hit in some places.

Bottom line:

Reducing superspreading events by avoiding the “three C’s,” Closed spaces with poor ventilation, Crowded spaces, and Close contact settings, have a dramatic effect at reducing the R0 of the virus, which, in turn, limits its morbidity and mortality. That is what the quarantine efforts have attempted to do. Certain countries around the world (S Korea and China for example) that have been very quick to identify and strictly control local outbreaks have been successful in reducing superspreading events. But, their strict measures are anathema to the psyche of the US. We prefer to deal more with the disease than the draconian restriction of our freedoms.

Other research reported in these pages has shown that liberal use of face masks can also reduce the R0 value to <1, which is the bench mark for stopping an infectious disease. Could liberal use of face masks be the happy medium for the US? Could it be a way to avoid draconian social and life restrictions while limiting the spread of the virus until we have an effective vaccine?

I believe so.


More Confusion About Hydroxychloroquine

After negative reports about the ability of hydroxychloroquine to help COVID-19 patients, and the FDA’s withdrawal of its emergency approval of the drug to treat the disease, we now get a report by the Henry Ford Health System that it was effective.

I am not sure what to believe about hydroxychloroquine at this point. I have seen and reported on convincing reports that it has a good effect in COVID patients and I have seen and reported on convincing reports that it does not.

Someone needs to sit down and look at all the raw data of all these reports to see if there is some trend that can explain it all. For example, what were the doses given in the different studies, what was the timing of the doses, how long was it given, what were the statuses of the patients it was given to, etc? If we weren't in such an understandable rush to find a treatment for the disease, all these things would be hashed out in a couple of large clinical trials over a couple of years. But we have been very rushed. For a drug that had clearly obvious effects, such confusion probably would not be a problem. But hydroxychloroquine does not seem to be all that obvious.

All of this tells me that if the drug is beneficial, it is for a select range of patients, or at a narrow therapeutic window, or both.

We will see.


Data Show That COVID-19 Is 50-100 Times More Lethal Than Flu

Using a calculation called the infection-fatality rate, paired with the past few months’ worth of data, health scientists are recently reporting that COVID-19 is around 50 to 100 times more lethal than the seasonal flu.

Early in the outbreak, scientists measured the lethality of COVID-19 using what is called the case-fatality rate—that is the number of COVID-19 deaths divided by the number of confirmed illnesses. But as we began seeing that there were many infected people who never got ill, people began pointing out that the death rate from the virus was much less than reported.

So, scientists have also looked at a similar, but more comprehensive metric: the infection-fatality rate. This statistical tool  divides the number of deaths by the total infection rate, including symptomatic and asymptomatic people.

Epidemiologists at Columbia University estimated the infection-fatality rate for New York City based on its massive outbreak from March 1 to May 16. Their results, published online as a preprint on June 29, show that the coronavirus was even more deadly than first thought. According to their data, the COVID-19 infection-fatality rate is 1.46 percent, or twice as high as earlier estimates (and much higher than a misinformed rate being widely shared on social media). This risk varies by age, with those older than 75 having the highest infection-fatality rate, at 13.83 percent.

In an analysis published on Medium, by University of Wollongong epidemiologist, Meyerowitz-Katz, compared the infection-fatality rates from influenza to several calculated around the world so far for COVID-19. Like COVID-19, influenza also has a high number of mild and asymptomatic infections. These cases are not accounted for in the majority of calculations of influenza severity made by the U.S. Centers for Disease Control and Prevention, which rely instead on hospitalizations, or case-fatality metrics.

Using a handful of studies that have calculated infection-fatality rates for seasonal flu, Meyerowitz-Katz determined that somewhere between 1 and 10 people die for every 100,000 that are infected with influenza virus. For COVID-19, that number ranges between 500 and 1,000 deaths per 100,000 infections. By his calculations, the coronavirus is likely to be 50 to 100 times more deadly than the seasonal flu, which supports the Columbia University findings.


The Common Cold And Rumors Of False-Positive CoV-2 Tests

Rapidly spreading rumors on social media are claiming that the recent increase in coronavirus cases in many states is the result of false positive tests due to the common cold coronavirus.  

This is NOT accurate.

This rumor fails to distinguish between antibody testing vs testing for the virus itself. Both tests are being done and they are not carefully reported and distinguised in the press. Antibody tests are being done by epidemiologists who want to know how far and wide the virus has spread and to know how many people exposed to it do not get sick. The antibody test does not determine whether someone is infected.

“Antibody tests” looks for antibodies to a coronavirus in a drop of blood from a finger stick, and they simply determine whether or not you have been exposed to a coronavirus. They do not say that you are currently infected with it. And a positive antibody test could be due to the CoV-2 virus that causes COVID-19, or it could be due to a coronavirus that causes about 30% of cases of the common cold. This test is NOT used to diagnose a current CoV-2 infection, it is just used to measure how many people have been exposed to the virus. Viral antibodies can linger for a few weeks after you clear the infection.

Positive antibody tests are not what health agencies are talking about when they say cases of COVID-19 are increasing, or when they say the incidence of infection is increasing.

When health experts say “cases are increasing,” they refer to cases of diagnosed COVID-19 illness. When they say that the incidence of infection is increasing, they mean that the number of people actively infected with CoV-2 is increasing. These are the numbers we should pay attention to when talking about the spread of the pandemic, not the antibody tests.

In contrast to antibody testing which just shows whether or not you have been exposed, health care folks detect active CoV-2 infections by taking a nasal swab that picks up virus budding from cells in your upper respiratory tract. They then use a highly specific and highly sensitive molecular test called RT-PCR, that your humble correspondent helped develop, to detect the presence of the viral genome.

This molecular diagnostic test, along with a clinical diagnosis of COVID-19 disease, are what people generally refer to when they say that the coronavirus is spreading.

Admittedly, the press too often does not distinguish whether they are talking about increasing antibody tests vs increasing clinical and molecular diagnoses. This contributes to some of the confusion leading people to leap to the unwarranted conclusion that it is a common cold, rather than CoV-2, that is spreading.

But, they are still wrong.