By Vinay Kolhatkar
April 20, 2020
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.
“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.
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.
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?