We spoke of opening schools yesterday.  The consideration has to include the fact that seemingly healthy folks are absolutely capable of infecting others.  As a matter of fact, we know that little kids harbor more viruses (10 to 100X more!) in their upper respiratory tract than the rest of us- which means they are MORE likely to infect  the rest of us.  And, asymptomatic folks (which seem to equal about 30% to 40% of the population harboring the  coronavirus) have the same viral load in their respiratory tract as those who manifest symptoms.

The only saving grace is the asymptomatic folks are not actively coughing or sneezing.  So, they may expectorate fewer viruses.

Yet, there are still other issues.  We tell folks to quarantine for 14 days if they’ve been exposed to someone with COVID-19/  But folks who manifest symptoms still test positive for 20 days; that number is 18 days if they are asymptomatic.   Uh,oh- some folks persist to shed viruses for 30 days!   (Yeah.  I always wondered about that 14 day quarantine.)

And, then, we don’t know how long the antibodies to the novel coronavirus survive in our bodies.  Two months?  Six months?  A year?  Forever?

It’s also possible that the asymptomatic folks had active T cells, part of our immune system, that recognized the SARS-CoV-2 due to exposure to other coronavirus (MERS, SARS, maybe even the common cold).   And, those T-cells managed to prevent the infectious viruses from leading to COVID-19 manifestations.  (This would explain why 20% of those living in various New York communities appear to be immune to the disease.)

Drs. Shane Crotty and Alessandro Sette (along with a slew of others) published their results, Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals in Cell.  When comparing the blood of those who recovered from COVID-19 with older blood samples (2015 to 2018), they were amazed to find that the blood from at least 40% of the older samples clearly recognized the SARS-CoV-2 virus.  Remember the older samples predate the finding of the virus!  (This finding has since been duplicated in more studies.)

And, here’s where I will be proposing an hypothesis.  (That means I lack sufficient data to claim this is true!)

We know that vaccinating our kids (and me) against diseases demonstrates some very funny effects.  The smallpox vaccine provides some protection from measles. So, finding that recently being inoculated against pneumonia reduces the risk of developing COVID-19 by about 28% doesn’t seem so crazy.  But, a recent polio vaccination yields a 43% risk reduction against COVID-19.

That may explain why little kids seem to be ‘immune’ to COVID-19.  After all, they recently did receive the polio AND smallpox vaccinations.  Given these ‘stimuli’ may explain their asymptomatic behavior.  The polio and smallpox vaccines yielded sufficient T cell immunity for their bodies to resist the viral loads of SARS-CoV-2.  (That’s my hypothesis!)

Then, we have the unusual behavior of asthma sufferers.  They seem to be less likely to contract COVID-19.  Here’s another hypothesis.

We know that ACE2 receptors (in healthy folks) maintain stable blood pressures.  And, that’s the receptor to which the SARS-CoV-2 latches.  But, folks with asthma have reduced levels of the ACE2 receptors.  And, when exposed to allergens (things to which they are allergic), there’s a further reduction in ACE2 receptor levels.  Which may explain the anomalous fact that asthmatics are less likely to manifest COVID-19.  They have a lack of available ACE2 receptors upon which the coronavirus may latch.

And, one more fact (this is NOT an hypothesis) before we burst a few bubbles today.

Researchers at Mass General, MIT and Harvard, and the University of Washington (UW) School of Medicine, along with Serum Yx System [Cambridge], wondered whether there was a way to discern who would succumb to COVID-19 and who would achieve successful convalescence. (Galit Alter, PhD of Mass General/MIT/ Harvard Med and Helen Chu, MD of Washington led the study to be published in Immunity.)  As such, they examined the antibody formation in hospitalized patients (and a matching cohort).  It seems that there are five markers (of immune response) that may be the key.  Moreover, this data could help direct the development of potential vaccine candidates.

The SARS-CoV-2 virus has two primary proteins that are responsible for triggering immune responses.  We are all familiar with the spike (S) protein; the other one is the nucleocapsid (N) protein.  (The nucleocapsid is the ‘shield’ of the virus- it protects the viral DNA.) . The N protein that doesn’t produce virulent antibody response is more prevalent in the coronavirus, though.

And, that was the key. Folks who responded to the N protein (IgM, IgA2, and antibody-dependent complement deposit) were less likely to survive the infection.  It’s the response to the S protein (IgM and IgA1) that yields the anti-COVID-19 results we need.

This finding needed verification.  So, the researchers tested 40 other folks (20 convalesced, 20 deceased) from a different hospital.  And, the results were duplicated.

At the very least, we need to find a way to attenuate our response to the nucleocapsid.