- #51
Paul C
- 12
- 3
Phil Core said:
A couple of thoughts.
A full and complete examination of the virus' RNA chain is exhaustive. A 30K base transcriptome offers a vast number of post-translation possibilities, in accord with host cell interactions. It's one thing to count bases or discover and illuminate the function of exon/intron regions, but once proteins are translated, hydrated, and start folding their angles are less straightforward. The nice thing about discoveries in molecular biology is that they come steadily and across disciplines, so an enzyme can be characterized in one species and a similar sequence can be found in an entirely dissimilar species. A chimeric RNA, suggests the article, implies more than one strain became simultaneously able to infect humans from reservoirs in different species. I think this view is overly complicated. Here's what I think happened: Through repeated and chronic exposure to animal virus reservoirs, our human responses to foreign matter withstand innumerable contacts with microorganisms. One occasion, though, a human host for whatever reason responds to viral RNA. Perhaps his cells' polymerase generates a few copies of the virus, a few enzymes, maybe makes it to a Golgi body where it is encapsulated and released. Henceforth, we've a virus that has characteristics amenable to re-enter healthy human cells and begin the cycle again.
On the subject of reverse trans DNA, I believe I heard yesterday this was one method under study, as an antisense marker of known SARS CoV2 sequences. The stereochemistry of such an approach is beyond me, but DNA is well characterized and quite stable as a reagent, so I gather that's a design that holds promise.
I'm wondering what proportion of seropositive Covid-19 patients are actually killed by influenza, and are patients routinely screened for the flu? Because, the threshold for concern with Covid-19 is so low!
Best wishes.
