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Native Answers Coronavirus Related Basic Science Questions

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This schematic goes well with testing. The exact SARS-CoV-2 timeline has yet to be worked out. But red line is what the RT-RPR test is going to detect. You get an idea of the window in which infection can be determined to be active.

Also show you why antibody testing doesn't do any good for monitoring disease with goal of self-quarintine/isolation and contact monitoring. It won't be detected until viral spread (day 5 in this diagram) threat is mainly over.

IgM tests often lack as good as specificity as an IgG test, because they are less specific antibodies in general. But you see they peak first at roughly day 15.

IgG peaks latest and has ability to be lasting. Are they good antibodies for protection? That is the question.
 


Very nice blog post out of Dartmouth. Risk assessment of a lot of behaviors related to getting infection. Talks of infectious doses, droplets, surface contamination, etc.. Also has some good considerations and models on reopening.
 
I still take questions, but hard to have concrete answers as we deal with a public policy nightmare.

1. Still true that the majority of adults will get COVID sooner or later? I recall early estimates of 80%.

It would seem to me that barring a vaccine, and the degree to which the infection in the community that a high percentage will become infected. 80% makes sense if you go back and look at herd immunity modeling. Basically there are enough immune people that are blocking spread of the infection by not becoming sick themselves they prevent the spread of disease once the population is nearly saturated. All of this depends on the development of "durable immunity" or lasting protection, whether that comes from a vaccine or natural infection. Unfortunately that hasn't been determined at this point. My GUESS is that the natural infection is potent enough to be leading to lasting immunity, however, mild cases may not achieve that. Science on that topic is still unresolved at this point.

2. I've believed that – if contracting COVID is inevitable – getting it later is preferable to getting it sooner. Is that a productive assumption?

Interesting proposition and answer potentially differs if you are thinking on an individual level or a societal one. I can come up with arguments/examples both pro and con. Early infection, got it done with and over. Maybe immune. Thats nice. Medical care still working out treatment protocols and societal fears are high. Society, wants the slow infection, less taxing on healthcare system, though I believe we are pretty well ramped upon on goods/supply front.(ventilators are able to be distributed to hot spots). Example, from influenza (1918 pandemic), later was bad, after 15 or so generations, or passages through individuals, host adaptation was maximized and disease much more devastating. Personally, given the mutation rates and mechanisms of replication, SARS-CoV-2 is much less likely to do this and the mutations this far with the recent uptick aren't quite the same as with the 2nd wave of the great influenza. So basically, if know going to catch it, it is 6 of one and a half dozen of another on the timing.
 
I assume most of you have seen articles about vaccines in trials and success rates etc. Supposedly 139 vaccines in phase 1 trials and others moving forward. The Moderna vaccine had positive results in small sample size and relatively young population, with 2 doses of the vaccine. There was an immune response of "Neutralizing antibodies" which is good, because it is possible to have an antibody response that is not protective. The article states the results mirrored the pfizer vaccine results that released in early July. So there are a couple of options.

Now, for the curious, this Moderna vaccine is pretty sweet. It is an RNA vaccine. There are currently ZERO approved RNA vaccines. Should be a strike against it until you understand the technology/mechanism of the vaccine, in which case, you are like dayum!

So in trying to be simplified terms. RNA is put in liposomes and injected. liposomes fuse with human cells and the RNA is inserted into the cell. RNA is not what antibodies are formed against however, this RNA is modified for stability and increased expression of protein. In doing so, the RNA is cranking out a specific protein, (likely the Spike protein receptor binding domain, but I am not 100% sure on that). In doing so, our own cells are producing a protein that is foreign and our bodies create antibodies to it. This process is more efficient as protein made inside the cell more naturally mimics an infection allowing protein presentation to the immune system. Except you don't have the other immune stimulatory negative effects and the RNA lacks the ability to replicate and spread, so there is no risk of infection or mutation allowing an attenuated viral vaccine infection to revert and cause disease.





RNA vaccine summary. (not Covid specific)

 



Is anecdotal and negative data... but is pretty compelling example of mask effectiveness.

TL;DR. Two mask wearing/covid positive hairstylists in MO did not spread covid to ~140 customers.

 
This is a good thread for anybody who wants to understand a bit more of the immunology. And honestly, you probably need a decent amount of immunology to get through this. The thread is actually still being made, so I'll have to come back to fully update the summary.

TL:Biggrin:R or o_O

Most people who have had a covid infection made antibodies that were "neutralizing" aka protective. There is some decrease in levels of antibody overtime, but author thinks normal, and likely protective. Also states further testing will be required to actually get that nailed down.

 
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Nice summary of RNA vaccines and their utility.

 
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