A single line often inverts meaning once you see what it
answers, so neighbouring messages are always shown.
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2. The UK variant is important on many levels, but I believe relates directly to the PO of SC2. I don't fathom themechanisms, [maybe there's a precedent in noros or elsewhere] but it looks like the mutations in RBD and the FCS and elsewhere are "coordinated" in some way. The closest correlate I can think of is when you get a mutation in one part of protein you often get a compensatory mutation in another part of the protein - sometimes thesecompensatory mutations interactin the secondary or tertiary structure, but often not so much.https://pubmed.ncbi.nlm.nih.gov/17507468/ or better here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1599768/[check out the editor].
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3. As for the FOI from the USRTK group, which I believe has its roots in the antiGMO cabal - along with right wingers(Bannon/Yan/FOx news) and the out-of-their-lane amateur detectives/DRASTIC. we are up against a lot of people trying [and failing] to tear us down.
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@Robert Garry 2) - I am now utterly convinced it is transmitting faster (I may still be wrong but all the data is pointing that way - and I am super cautious about these things). I think the RBD + furin site must be a top combination. Possibly the 69-70 & 144 deletions just to tune things a bit.
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But I think it probably got selected for higher infectivity within the chronic patient and then got out and took off.
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2020-12-18 07:08
Kristian G. Andersen
If it's from a chronic patient, probably also highly resistant to neuts. Any early data on that? Anything clinical?
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Speaking of which - this is good. https://twitter.com/jbloom_lab/status/1339939720558563328?s=21
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My follow-upon 3. It seems to me that one of the major hang-ups is: "you can't rule out lab escape." The problem isthat lab escape has several levels of crazy. Level 1a. full-blown sc2 was brought into the lab from someone notpracticing good ppe. s/he got infected in the cave. We all agree that this is possible but compared to all the other bat-human exposures the odds of this are very low. It also assumes that 100%SC2 is already in a bat. Also assumes either that the nonPPE wearing pstdoc never got sick and or that the virus was isolated and covered- up, which isobviously ridiculous. However, the RaTG13 is "fake: crowd which apparently included Frankie/Alina believes that RaTG13 SRA were contrived to cover this up. Total Bullocks. Level 1b. SC2 exists in some other species and byluck a laboratorian caught one of these animals and started the transmission to other humans. This has even lower odds compared to all the other animal-human interactions. Level 2a. presc2 [99%] brought into the lab and modifiedby seamless engineering. Level 2b presc2 [99%] brought into the lab and modified by cell culture or animal passage. Level 2 assumes a very close relative to SC2, which would have obviously been a big story, but then held up for GOF research. Again, the conspiracy theorist thing that Eddie and other made up the pangolin viruses and RatG13to cover this up. Levels 3. sc2 stitched together by combining parts of unreported sarbecoviruses and modified byseamless engineering. This assumes that WIV had the GD pangolin virus sequences or something similar from another animal (bat or other) and that they combined these viruses to create SC2 - this is the Yan/Bannon/Fox nonsense, but in reality it is not that different to what Alina/Drastic etc are proposing. Yan just made the mistake ofputting a flowchart on paper which is obviously loonie.
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Agree Andrew that the NTD deletions tune things up. I do suspect as I wrote before that the NTD is likely involved atleast in some early cell interactions, if not interaction with a full-blown receptor.
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Yes - beautiful and important work out of the Bloom lab - very relevant. Agree that the chronic patients are an unanticipated wild card. Selecting for higher infectivity: it's the whole macrophage tropic HIV get replaced by T-celltropic HIV story again. Immunocompromised patient makes the story even more symmetrical.