The Pandemic: Cardinal Numbers No One Talks About

It’s plausible that somewhere between 100 million and 500 million people on earth have had, or are having, the coronavirus infection.

That is a staggering statement when, as at April 19, 2020, the confirmed cases numbered 2.35 million. And we are projecting that somewhere between 40 to 200 times that, is the real number, which is between 1.3% and 6.5% of the world population.

What’s the reasoning behind how we may have gotten there? And what’s the evidence?

Let’s go through the reasoning first.

The Presence of a Virus Is Not a Presence of Sickness

SARS-CoV-2, aka coronavirus, aka SARS-2, is not the same as COVID-19, aka C-19. The former is the virus, the latter is the disease that one may get from it.

Human beings have an immune system that resists or controls viruses that invade or reside in their bodies. Writing in The Scientist, Professor Eric Delwart, who investigates human and animal viromes, says [emphasis mine]:

Most viruses are neither consistently pathogenic nor always harmless, but rather can result in different outcomes depending on the health and immunological status of their hosts. The less pathogenic a virus is—the lower the percentage of infected people who become sick—the larger such case-control studies need to be to detect a difference between the groups.

Given the large number of viruses detected in healthy hosts, it is likely that some of the viruses initially found in sick hosts are simply harmless coincidental infections.

Even a small viral load may be detected in a diagnostic test. But the host may never get sick.

“Viral load” is the term virologists use to denote the strength of the virus—is it an army of thousands, or an army of millions? Higher the load, greater the chance the virus may win the battle. Then the immune system must bring in the artillery—for example, by increasing body temperature, so as not to lose the war (death).

Even a small viral load may be detected in a diagnostic test. But the host may never get sick.

On April 15, Boston25News said this of the tests carried out in a homeless shelter:

Of the 397 people tested, 146 people tested positive. Not a single one had any symptoms.

“It was like a double knockout punch. The number of positives was shocking, but the fact that 100 percent of the positives had no symptoms was equally shocking,” said Dr. Jim O’Connell, president of Boston Health Care for the Homeless Program.

Exponential Testing

The global “confirmed cases” daily number had been growing until April 11. On March 1, there were 1823 new cases confirmed, and on April 1, 74,407—40 times as many.

The media told us that this is an exponential growth in infection.

But that increase in detection (confirmed cases) from March, 2020 is positively correlated to the number of tests performed. See the plot of tests per confirmed case in Our World in Data—most countries were not testing much, if at all, before March 2020.

But detection is not the same as occurrence. When did the virus contagion begin? Not when tests began—that’s when the media started lecturing us 24/7 on the stats.

But detection is not the same as occurrence. When did the virus contagion begin?

Not when tests began—that’s when the media started lecturing us 24/7 on the stats. The virus commenced its worldwide spread at least as far back as December (possibly November) 2019. But the late-2002 SARS-1 China was not the same as the late-2019 SARS-2 China, in terms of its booming middle class traveling overseas, the 50 million overseas Chinese citizens making home visits, and the ugly coincidence of the Lunar New Year celebrations in January 2020.

One recently published study asserts that SARS-2 (coronavirus) is contagious even when the host is largely or wholly asymptomatic.

Surely, SARS-2 must have spread like wildfire during those heady, wintry days when no one was practicing social distancing—we even had Christmas and football and concerts and parties before March 2020, and we also had packed subways, sweaty nightclubs, and smoky bars, all filled with bodies without face masks. This period—the three northern winter months, must have been when the exponential growth in infection actually occurred.

But the hospitals were not overwhelmed back then, except in Italy (refer our Coronavirus Special Edition for why Italy is an outlier). Could it be because a vast majority of cases had nil to mild symptoms? Perhaps the symptomatic thought they had the flu. Deaths may have been attributed to respiratory illness. Maybe a large majority never knew they had the SARS-2 virus.

But hosts produce antibodies after a few days of infection—some (IgM) suggest an infection is ongoing, while some of them (IgG) stay long after the infection is resolved. Such antibodies can be detected by serological tests—lab analyses of a blood sample.

Antibodies that stay long may lead to some level of immunity. Evidence suggests that the immunity to SARS-1 and MERS after an infection was around three years, although for SARS-1, the antibodies may persist for twelve years.

To date, reinfection cases of SARS-2 are so low that they could be attributed to false tests. What’s unknown is how long the SARS-2 term antibodies last, and to what extent they provide a defense against a new infection—do they make it impossible? Or highly unlikely?

The Evidence

Preliminary results of some serological studies are in.

Initial findings of one study indicate that between 48,000 and 81,000 residents in Santa Clara County, California, had antibodies as of April 1, 2020, back when the official count was 956. The infection number is extrapolated from a sample of 3,300 residents tested. The results had to be adjusted for the sample’s demographic not being reflective of the county. Hence the wide range—50 to 85 times the official count. Nevertheless, the gap is phenomenal.

As tests for the presence of the virus become more widespread, that gap could narrow. Let’s assume the gap is currently 50 times.

As at April 19, the official count of cases in the United States was almost 739,000.

If we assume that the county is reflective of the country in the ratio of real to official count, then almost 37 million Americans (50 times 739,000), or 11% of the population, may already have antibodies for SARS-2. This 11% is much higher than the range in the county, because the official count per thousand in the county is much lower than in the country.

Now here’s a paragraph from that American study that leaps out:

Several teams worldwide have started testing population samples for SARS CoV-2 antibodies, with preliminary findings consistent with a large under-ascertainment of SARS CoV-2 infections. Reports from the town of Robbio, Italy, where the entire population was tested, suggest at least 10% seropositivity; and data from Gangelt, a highly affected area in Germany, point to 14% seropositivity.

Are some countries already at a “herd immunity” level of 10-15%?

Are some countries already at a “herd immunity” level of 10-15%? Our staggering claim at the top had a 6.5% upper limit on the global number (200 times the official count), but, arguably, in highly populous countries like China and India, where testing rates per million are lower, that gap could be appreciably larger than 50 times.

Deaths

The U.S. coronavirus death count of 39,000 as at April 19, 2020, may be missing deaths attributed to pneumonia or respiratory illness during those three deadly winter months when no one noticed a shortage of ventilators, ICU beds, or unusual cases of pneumonia.

During those three deadly winter months no one noticed a shortage of ventilators, ICU beds, or unusual cases of pneumonia.

But in April, we also had the instance of New York City Mayor De Blasio “allocating” more deaths to C-19—an increase of 3,700 people, or 17%.

Dr. Annie Bukacek alerts us to the fact that deaths are being attributed to C-19 even if SARS-2 was not definitively the precipitating cause—she says the CDC puts both true C-19 deaths and speculative guesses on the same footing. Even if SARS-2 was not detected in a test, even if other pathogens (such as influenza) that may have been precipitating causes were never tested, even if a person on his deathbed from lung cancer acquired (or was suspected to have acquired) C-19 in hospital from being there during his last days, it could be counted as a C-19 death.

But despite the political reasons the death count may be overestimated, let’s just take the official count, and “allocate” yet another 11,000 deaths to it, shall we, to make it 50,000.

If indeed 37 million Americans have had a brush with SARS-2, then the death/exposure ratio is 0.135% (50,000/37M). Dr. Jay Bhattacharya, one of the architects of the Santa Clara study, is also suggesting a death rate for SARS-2 of 0.1% to 0.2% (one to two in a thousand), which is of the same order of magnitude as influenza.

But What if SARS-2 Is Cleverer than SARS-1?

Business Insider’s recent SARS-1 story in pictures reveals eerie parallels with SARS-2:

In 2003, SARS-1 originated in China’s wet markets, China kept it hidden from WHO for several months, then a whistleblower doctor wrote to international media, and from Room 911 (indeed) in a hotel in Hong Kong (now renamed Hotel 911), the virus flew out internationally.

But there’s one striking difference.

Virologist Peter Kolchinsky’s Twitter thread, based on the paper submitted to Nature, contends:

SARS-1 was a comparatively dumb virus. It went straight for the lungs, announced itself before it could spread to others, and so got social distanced into extinction. But SARS-2 is stealthier, spreading first before revealing itself (and causing harm).

This virus has an incubation period (from infection till symptoms appear) of up to 14 days, and in rare cases, longer, but asymptomatic contagion can occur.

It must be that in many healthy hosts, infections are resolved with nil to minimal symptoms.

But this aspect only makes early quarantining and contact tracing that much harder, and reduces the effectiveness of partial lockdowns.

And, the phenomenal disparity (50 to 85 times, 10-14% of a population) suggests that not all asymptomatic cases are in an incubation period. It must be that in many healthy hosts, infections are resolved with nil to minimal symptoms.

Inferences: The Numbers and Tests We Really Need

Stat News reported back on March 10:

We can expect a doubling of cases every six days, according to several epidemiological studies. That means we are looking at about 1 million U.S. cases by the end of April; 2 million by May 7; 4 million by May 13; and so on.

As the health care system becomes saturated with cases, it will become increasingly difficult to detect, track, and contain new transmission chains.

Stat News subtitled it “Some simple math offers alarming answers.” But the media’s “simple” math assumed that 14% of infections would become severe, and that 6% would need hospitalization. The simple math was based on what China submitted to WHO. But China, too, was probably missing millions of asymptomatic infections. The calculations used to recommend lockdowns may be off by orders of magnitude.

The horse may have bolted back in December 2019. Shutting the gate partially in March 2020 was ineffectual for contagion containment. Nevertheless, economic suicide was never justified. In developing countries, e.g., India, where interstate migrant workers need casual work for survival, where city public transport is so crowded that contact tracing is beyond impossible, where child malnutrition and other infectious diseases take a much bigger toll, any lockdown is exceptionally counterproductive.

Now only herd immunity, obtained by exposure to the “clever” virus or the vaccine, will end the war. Workplaces may need to insist on protective gear and social distancing—our immune systems have a better chance of beating a lower viral load. And the vulnerable should isolate themselves. People testing positive to the virus should also isolate themselves.

But a test that reveals we were free of this virus yesterday is no guarantee that we are free of it today—the negative test has no value for our ability to roam freely. What we really need to know is whether we have long-term antibodies.

It’s time to focus on a new set of numbers.

Serological tests also help get estimates of herd immunity levels in various populations, which can put international airline travel, concerts, and nightclub reopening on a much sounder footing—“no new cases for a week” in a shutdown area could hide many of those 50 times asymptomatic carriers roaming around.

It’s time to focus on a new set of numbers.

This essay benefited from comments made on a previous draft by Donna Paris and Walter Donway (Savvy Street), and Dr. Bhalchandra Kulkarni (Consultant Surgeon, Dhanvantari Hospital, Nashik, India).

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About the Author: Vinay Kolhatkar

Vinay Kolhatkar is a freelance journalist, novelist, screenwriter, and finance professional. He is the Chief Editor of The Savvy Street. Vinay has authored a TV pilot screenplay Undercover: The Story of Jamila, and two literary thrillers A Sharia London and The Frankenstein Candidate.. He is also the co-author of Media Wars: The Battle to Shape Our Minds. More about Vinay is at the Founder page.