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.What, having a previous disease might make you immune, or at least resistant to new disease? What a novel thought!
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.
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.
Well, not exactly. In fact the original vaccine against Smallpox was developed based on Edward Jenner's observation that milk maids, who commonly caught Cowpox (which turned out to be a virus related to Smallpox) did not commonly catch Smallpox during epidemics. In fact, the very word "vaccinate" come from Vacinnae, which was the medical term for Cowpox, as compared to Variola for Smallpox.
If true, this would also point to research lines for a vaccine for multiple coronaviruses.
Don't bet your life on this because I said so.
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