Private channel session 930
23 messages over 3h 20m, 2021-02-06 – 2021-02-06.
A “conversation” here is an activity session — a run of messages with under 60 minutes of silence inside it. The channel had no native conversation boundaries.
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The question is how much we want to directly enter the fray? I was quite happy with just talking about the natural origins based on the available bat and pangolin sequences but obviously that doesn't address these arguments. Ifwe want to go full on to attack these ideas I think we have:1. You can't go from RaTG13 to SARS-CoV-2 by passaging. Require the induction of 1200 mutations, about half ofwhich are reversions back to the common ancestor. Even if you did it, that would be a shit load of passages sowould be unfeasible in animals. And passaging SC2 in cells causes all sorts of stuff to happen like loss of FCS (although perhaps that is just some cells).2. You can't use modern molecular techniques to create this virus 'de novo' because you have no idea what mutations you would put in. You still need a starting virus that is almost identical to SC2 and just introduce a few things (i.e. FSC and the odd ACE2 contact residues). And you would introduce the perfect cleavage site and theoptimum RBD. So this means something almost the same as SC2 exists or existed in a lab without any publication.3. The only plausible lab origin theory (and possibly the only one that isn't a conspiracy in the event itself) is that someone collected SC2 as part of a collection of samples, was working in through them perhaps to isolate orsequence them and infected themselves (without knowing) and then transmitted (without knowing). But this is simply specific subsection of the zoonotic hypothesis - no different from bat->farmer->market worker. Given it isspecific and this would afford a single unique opportunity for the virus to jump, it is vanishingly less likely than the other types of contact humans have with animals.
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Damn you are good - so well stated Andrew!
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:beer:
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For #3 I would add that Alina, Baker et al have recommended stopping all these activities, which of course is 180degrees opposite to what needs to be done. If you want to leave the world completely vulnerable to SARS3, SARS4 etc, sure stop studying sarbecovirus diversity.
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The way to do it may be to leave them with a couple of very specific things that they need to prove if they are to turn out to be right - the major one is that a live virus, collected from the wild, that was SARS-CoV-2 or near-identical to itwas in a lab in Wuhan in November 2019. Then just let them obsess about that whilst everyone else moves on. The problem at the moment is that they say all these vague notions about passaging and engineering that seem plausible to people who don't know what is required.
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Yes indeed that---is--- it! It's #2 aka Relman - and the pure essence of a conspiracy theory - they have the progenitor and are keeping it a secret because they don't want the world tp know they f'ed up and released it or they are hiding their super secret bioweapons program.
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No point in spending time explaining it's _not_ a lab escape - just keep reiterating the data supporting it's all natural evolution. Then combine that with three main things (1) lab escape proponents have not put forward a testable hypothesis, (2) the lab hypothesis comes down to a single 'fact' - this happen in Wuhan (that really is all there is toit), and (3) - and while I hate this part, it's effective - they're amateurs. It's not a nice look to be the person calling other scientists idiots, but they are - so I have no issue hammering on #3 these days.
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The only viable version of the "lab escape" hypothesis that's left, is the one we mention in PO1 - that somebody had the virus at the WIV and popped it into tissue culture. But as we say, that would look identical to natural emergence -no point for scientists trying to figure out if that could have happened, since it's not a scientific question - it lies with intelligence.
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Exactly - that was my point 3.
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But that is not the hypothesis they are proposing.
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But in the end you are never actually trying to convince these people, just make their arguments seem daft.
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Do they have an actual hypothesis?
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"just make their arguments seem daft" Excatly
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And when you break it down - all they have is the fact that this was detected in Wuhan. That's literally it.
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Yes.
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And that is why they are so anti any idea of a previous history of circulation or cases in Europe in November etc.
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Alina is still in love with her notion that the virus was "already well adapted to humans" when the first cases were detected based on dN/dS. Yet, we know the virus infects minks, ferrets, dogs, cats, lions, gorillas, rodents as well asit infects humans. Doug and the VoC that have followed show that SC2 and its RBD and FCS are still adapting to us.
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I think they forget that SC1 != SC2. They're literally basing that entire argument on n=1. I told her this many many months ago (gave her an example from Ebola - which looks like SC2.... mysterious!), but I guess it doesn't fit the narrative very well.
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Do you remember the big deal that was made about how Shi did not mention the FCS in her first SC2 paper? Did I miss it? Where in the Chan-Ridley paper is the mention of the FCS that definitely proves SC2 is man-made?
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Guess they forgot FCS too.
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Moving the goal post. Constantly.
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Speaking of FCS https://www.sciencedirect.com/science/article/pii/S1873506120304165 YP_009072440.1
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_Hibecovirus - two known One with a FCS the other not. the S2' of the nonFCS one has a predicted O-linked glycan...._