Private channel session 1009
23 messages over 1h 9m, 2021-02-21 – 2021-02-21.
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.
-
Did you see this: https://www.biorxiv.org/content/10.1101/2021.02.13.431090v1.full.pdf+html
-
I've not read it carefully yet, but interesting to see the adaptive changes in ORF1ab as well. They are dead right thatdN/dS is pretty rubbish when you have fixed mutations.
-
Yeah, just saw it too - pretty interesting. And yes, "A" is totally unique to SC2 there
-
I'm in...sorry, just catching up this thread now.
-
it's nicely spotted, since it's the only mutation unique to SC2 in the RBD - we should have picked this up earlier. Iwonder if H519 does something interesting too.
-
519 is "H" in SC2, but N in almost all other sequences - the only other deviation is K in the P378 pangolin, although that is a pretty bad sequence, so might not be real.
-
No one thinks about fixed changes: nicely blows-up the idea that SARS-CoV-2 was perfectly adapted to humans at the outset.
-
Well, actually, this supports being perfectly adapted to humans :wink:. A in that position was fixed from the get go.
-
(and yeah - dN/dS is shit. Just no point).
-
I can certainly see that Doug & Phil increased transmissibility, but that does not explain why B.1.1.7 et al.,which arose later, are doing so well. That may have arisen through an intra-host advantage, but it's obvious that they have an epidemiological scale advantage as well. Clearly they have increased fitness which can only be due to (i)increased transmissibilty in itself....which suggests that there should other key mutations in ORF1ab (?) and/or (ii)immune evasion that enables more refection and hence increases R. Perhaps that deletion in nsp6 is the key?
-
Are there *proportionately* more chronic infections? Do we know their overall frequency?
-
Definitely needs to be set out here.
-
The Chan/Petrosky analysis was that dn/ds suggested that there was NO adaptation to humans. This shows otherwise. We know that this mutation is fixed in all the human samples studied to date, but we don't know about any chains of transmission that died out.
-
Hmm. Not sure about this paper - they are using software for detecting genomic selective sweeps using LD, I think.
-
But they do then do experimental assays to confirm these computational results. I can't judge how good these are. The bottom-line that there has been a continual adaptive process.
-
Yeah, the sweep analyses are shit - can't do that in viral genomes, only sexually reproducing organisms. That said, they DID come across a very very interesting mutation (by chance?) and the experimental data is good
-
Yes, it's the experimental data that is interesting.
-
In other news: https://peterdaszak.com/
-
@Kristian Andersen You're included for your 'fairy tales'. Someone has put a lot of effort into this shit.
-
Well, they got my last name wrong so they can't be that clever... Unbelievable how much time some people have on their hands. [shared file(s): Screen Shot 2021-02-21 at 4.13.10 PM.png]
-
"PETER DASZAK MEMORIAL RESEARCH INSTITUTE". That's pretty good - I gotta admit.
-
... made with Microsoft FrontPage - oldskool.
-
Lots of young scientists are mentioned - pure evil I think.