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Of the five salient points they make here, I would argue that they are a lot less strong than the authors believe them to be. Point 1 can also likely be made f
by hirenj 6y ago
Of the five salient points they make here, I would argue that they are a lot less strong than the authors believe them to be.
Point 1 can also likely be made for the original Sars-CoV, and probably is irrelevant. If they show CoV-2 is more human like than the earlier, then they can begin to make the point.
Point 2 is a gigantic leap of faith - I don’t understand how they connect amino acid inserts into the sequence to gain of function experiments. It makes no sense!
Points 3 & 4 are related: The extra charge on the RBD. If you look at the previous virus, it has a much smaller positively charged patch, and this expands in CoV-2, which makes an evolutionary drift in this direction entirely reasonable. It’s not a wholesale integration of a brand new feature. This charged patch is actually important for binding to heparan sulfate, which gets involved with a bunch of viral entry events (eg AAV, Chinkunguya virus, some other coronaviruses I think). There’s a few recent preprints that discuss the HS relationship with Cov-2, and can go a long way to explain the tropism of the virus. The HS can overcome lower expression of ACE2, by possibly supporting the attachment.
Finally, point 5 is where they throw out DC-SIGN as a receptor. While there are high mannose glycans on the virus particle, I don’t know of anyone proposing this as a receptor for the virus. There is no biochemical/experimental evidence that they show to support this idea.
- DoingIsLearning 6y agoI will add a few points which I read on a github page and I am unable to verify, so I would be keen to have others review and sanity check: 1) The likely genetic source of SARS cov1 and cov2 is a species of bat in Yunnan province, thousands of miles away, two provinces away from Hubei (Wuhan). Ref: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5708621/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5708621/ 2) The outbreak allegedly started in December in Hubei province when the local bat population (which does not carry this SARS virus?) would be hibernating (?) 3) Only 66% of the initial 41 COVID patients had exposure to Huanan _seafood_ market. Ref: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30183-5/fulltext https://www.thelancet.com/journals/lancet/article/PIIS0140-6... 4) A seafood market where you would have to have non-hibernating bats from Yunnan thousands of miles away from Wuhan(?) 5) The seafood market is 13Km away from Wuhan Institute of Virology where Yunnan bats were studied. And 1.4km away from Wuhan's Centre for Disease Prevention & Control (?) Are these points real or misinformation? If real, why is there no pressure for an independent investigation?
- srg0 6y ago5) We're talking about a dense urban area ~ 1580 km^2. A _lot_ of businesses and institutions are within 13 km radius from each other. And there are 19 million people in this metro area. So a lot of things should e hapenning in the same city and only few km away, but most of them are not related to each other. 1, 2, 4) are probably irrelevant, because the researchers mostly agree that there was an intermediate host (which one remains to be determined, might be pangolin). So it doesn't matter if the bats were far away or hibernating. Consider also that people often travel, and trade is not limited to one town. 3) It only confirms that we still don't know who was patient zero, and when and where he or she was infected.
- DoingIsLearning 6y agoI suppose my issue here is that, all the point I mentioned appear to be inconsistencies with the current official statements and all the counter arguments deconstructed them are probability based and arguably as speculative as the authors claims on biogenisis.