Coronavirus and Covid-19 Rumination #5

By Rud Istvan – Re-Blogged From WUWT

The world continues to learn about this sometimes deadly new zoonotic virus. We know now from NYC that it is disproportionately serious in males (61% of tested symptomatics), more fatal in people over 65 (63%), and is disproportionately lethal (84%) in people with especially the comorbidities hypertension (55%), diabetes (35%) and obesity (50% of serious/critical [s/c] hospital admissions in NOLA, under 60 years old 2x s/c in NYC). More on the significance of these facts is developed below.

We know from two inadvertent extreme ‘lack of social distancing’ “experiments”, Diamond Princess (DP) and CVN71 (Theodore Roosevelt, TR), that only about 15% (TR) to 19% (DP, with several more weeks of exposure) ever test positive for the virus. That means that something like 80-85% of people have an immune system that seems to handle the virus effortlessly even in highly infectious, high viral titer circumstances–so that not even a positive viral shedding test develops. This could just be a very good innate immune system; it could also be a primed active immune system (i.e. the population was NOT naïve). A very plausible explanation hypothesis is developed below with important ramifications for opening countries from extreme lockdown measures.

We know from those same two ‘experiments’ that between 45% (DP) and 55% (TR) test positive but are asymptomatic. Now, some of that is just the now known incubation period with a mean ~5 days from infection and 97.5% displaying symptoms within 11.5 days. But we know also from South Korea that of the ~10600 now tested positive but asymptomatic and quarantined 14 days, that ~20% NEVER developed even mild symptoms. This is likely also explained by the naiveté hypothesis developed below.

In what follows, the primary technical sources are the Journal of Virology on coronaviruses, ncbi.nlm.NIH.gov for science publications, www.CDC.gov, and for clinical morbidity a very new ‘anecdotal’ survey article at Sciencemag.org.

Mitigation

The CDC says that there are four common cold coronavirus serotypes causing something between 15 and 35% of all common colds, (about 5% more are DNA adenoviruses that do not mutate much so immunity to them is long lasting), with the remainder caused by about 100 different rhinovirus serotypes.

For all three common cold virus types, the route of transmission is known to be cough, touching (handshake after cough), or hand face contact (cough droplets to a surface, touch surface, then touch mouth, nose, eyes.)  This is why common colds are only weakly seasonal while flu is strongly seasonal. That is why for COVID-19, social distancing, frequent hand washing, and consciously NOT face touching ‘work’. From a transmission perspective, Wuhan is ‘just’ another coronavirus.

An aside argued in rumination #4 and in other previous comments to others. Observational fact: flu is strongly seasonal, common colds are not. The reason lies in route of transmission. Inhaling infected aspirate principally spreads flu (aspirate particles are less than 5 microns). These aspirate particles dry out rapidly in dry indoor winter air (high surface to volume ratio) and remain circulating for many hours. In summer humidity, they don’t dry out and sink ‘rapidly’ to where they cannot be inhaled. Winter contact route of flu transmission exists but is distinctly secondary according to my personal communications with Dr. Fauci summer of 2009. Anything less than an N95 respirator will not prevent you from catching flu. Quarantine is ineffective. Annual flu shot is advised.

Now, there are two Covid-19 possibilities. Dr. Fauci might be right that it could be seasonal like flu, implying primary infection route would be inhaled aspirate. In which case, all the public mask nonsense is pointless. Or, it is ‘just’ another corona virus, the three recommended mitigation measures work, and public masks are still nonsense–unless you have active mild symptoms: dry cough plus fever >100.4F. In which case you should quarantine yourself and not be in public even with a mask.

Lack of transmission under extreme circumstances in 80-85% of cases

The four common cold coronaviruses are: 229E and NL63 in the ‘alpha’ serotype group, and OC43 and HKU1 in the ‘beta’ serotype group. Wuhan is also in the beta serotype group. All four common cold coronavirus spike proteins have two binding sites. In all four, the S1-CTD site binds the ACE2 receptor on epithelial cells such as line the nose, mouth, throat, and lungs. So their spike proteins, just like Wuhan, ‘key’ to that cellular receptor lock as well (as after being fully humanized) to another that varies. S1-CTD is a natural target for antibodies.

My naiveté hypothesis is that those exposed but not ‘infected’ on DP and TR may actually have been, but had a coronavirus common cold in the sufficiently recent past that their active immune system is NOT naïve thanks to S1-CDT. The antibodies simply clear the Wuhan virus before it can sufficiently replicate to even be detected. A lesser degree of immunity (older exposure) might allow the virus to sufficiently replicate to be detected, but not ever sufficiently to cause symptoms before the active immune system spools up to finally clear it.

If this naiveté hypothesis is correct, then the country should be opened immediately using the steps outlined by President Trump on Thursday. THAT is a HUGE deal economically. My hypothesis came about as I thought more about my vicious coronavirus cold referenced in guest post #1—without fever, so not Wuhan, but at 9 day duration plus more cough and less runny nose, also not Rhino.  Hence a personal recent experience motivation for rumination #5.

Clinical Morbidity

Age dependency is easy to understand. Older people have weaker immune systems and more co-morbidities.  Male dependency, dunno, just is.

Hypertension, diabetes, and obesity (in the under age 60 less impacted cohort) as the main co-morbidities take more thought to make causal connections, but can be explained with more scientific background knowledge.

We know from all the ventilator brouhaha that the primary Covid-19 clinical cause of death is viral pneumonia. The ‘ground glass’ in lower lung Xray is determinative.

But in ‘many’ cases, there are heart attack symptoms without coronary artery blockage, or cardiac arrest, or renal failure, BEFORE blood oxygenation failure, and without evidence for cytokine storms that would also damage other organs leading to a multiple organ failure diagnosis like in sepsis. And prior to death, there is in a very significant number of cases clinical evidence of kidney damage (e.g. bloody urine) and/or cardiac disfunction (e.g. arrhythmia, tachycardia). How can a respiratory virus cause those? The answer derives from the hypertension/diabetes/obesity clues.

Overweight (BMI>25) and Obese (BMI>30) is VERY strongly associated with both hypertension and type 2 diabetes according to the CDC. Hypertension by itself mechanically damages small blood vessels and capillaries. Diabetes by itself damages blood vessels and capillaries via several biological mechanisms.  The leading cause of death from diabetes (itself underlying cause #7 in the US) is cardiovascular in some form according to the CDC.

Now consider lower lung viral pneumonia. It starts when epithelial cell alveoli ‘air sacs’ are infected and eventually burst from virus. The active immune system attacks, scavenging dead and infected alveoli cells. Each single cell thick alveoli sac is intimately surrounded by capillaries; this is structurally how the lungs exchange oxygen into blood and CO2 out. That immune attack cannot avoid damaging these capillaries, already weakened/damaged by hypertension and diabetes. Now the Wuhan virus is in the bloodstream, not just in the lungs. And it turns out (from the biological role of the ACE2 receptor itself) that the heart and kidneys are the two other organs in the body with an unusually high concentration of expressed ACE2 receptor: in cardiac and renal cells. So it is clinically unsurprising that a lot of critical patients exhibit these other mortality modes before respiratory failure despite ventilators.

This also explains why a virus that cannot possibly be racist (despite DeBlasio’s politically inspired intimations this past week) disproportionately kills African Americans and Hispanics in NYC. Those racial groups have a disproportionate amount of obesity. See ncbi article PMC4265895 for NYC only details, or for all New York counties health.ny.gov.

CONTINUE READING –>

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