there's also nothing special about it being able to infect human cells at emergence... IT KIND OF HAS TO DO THAT IN ORDER TO EMERGE AT ALL, LET ALONE BE A PANDEMIC THREAT.
not to mention it's not unique... SARS Classic, WIV1, the recent Laos bat sarbecoviruses... all of these can infect human cells.
an "unbiased jury" would not claim it was created in a lab, b/c the scientific evidence plainly does not support that.
btw, claiming it was human-adapted at emergence is patent nonsense considering we got multiple progressively more human-adapted variants (B.1.1.7/Alpha, B.1.617.2/Delta) doing selective sweeps b/c they transmit better.
but more fundamentally...
...a virus w/*any* amount of pre-emergent human adaptation, passaging in humanized mice, etc, would have D614G at emergence.
it's a stabilizing mutation that in humans seems to be near-purely advantageous, is key to enabling later FCS improvements & has been picked up...
...in nearly every lineage, most prominently in B.1, of which nearly every virus in circulation nowadays descends from.
not having D614G at emergence when it got picked up & selected for near-instantly? yeah it was not human-adapted at emergence, just good enough.
as for the FCS, here's my thread on why this one does not bear any characteristics of engineering, just recombination:
our first speaker is Diego Forni & he'll be talking about how our 4 seasonal HCoVs arose! (a topic i myself have been quite interested in). #COVIDUnknowns
technical difficulties, b/c what would a webinar be w/o technical difficulties...
so i've been asked if it's likely that Ab waning is as likely after a third dose as it is after 2 & while it's suggestive that the answer actually is *no* (
) i also really think we're really over-focusing on the importance of this issue.
for starters, we're also dealing w/an antigenically drifted virus. it's not a huge case of nAb epitope escape, but L452R (& T478K too, to some extent) *do* affect binding somewhat. "waning" & the rise of Delta coincide, making it hard to tease apart how much each effect...
...contributes to a vax breakthru case. furthermore, B.1.617.2/Delta is very fast & replicates to a high titer very quickly, making relying solely on a memory response tricky if your goal is preventing infection or specially transient swab positivity.
going to assume this is about Jeremy Farrar's recent comment to the effect of having to expect another 30k dead/year in the UK from #COVID19... in which case, this won't be the case for much longer b/c this virus will run out of immunologically naïve hosts soon.
like hot take i actually agree with Ellie *if* this were a scenario we were talking about as likely (i genuinely think we tolerate too many flu deaths, for instance), but it's just not.
can we all seriously relax a bit instead of yelling at each other over hypotheticals?
also like, society is complicated & many pandemic restrictions *do* have externalities, often ones that can be hard to see. for instance, indoor dining restrictions in HK led to a massive increase in street sleeping. travel restrictions have caused hell for refugee applicants.
i've read a lot of #SARSCoV2 papers this year. i've even read a lot of *good* #SARSCoV2 papers this year. this is hands-down the best one i've read this year (yes even w/4.5 months left this year).
it was the subject of his @NIDO20201 talk, which due to technical difficulties had to be uploaded later, & so i never did a livetweet. so having read the paper extensively, i'll do a summary of it & some implications.
first, a bit of background: viral fusion proteins exhibit various metastable points along a tradeoff between fusion protein stability & fusogenicity.
a highly fusogenic protein will be excellent at cell entry but be highly unstable in even slightly harsh conditions.
i think a lot of people are misunderstanding the mechanism behind "shift to endemicity" in a CoV.
it's not at all due to the *virus*. yes, endemic HCoVs have certain mutations (such as a preference for closed RBDs on Spike where the CTD is the RBD) but those are from...
...selection pressure *once in the endemic state*.
what causes the shift is the virus going from antigenically novel to us having prior immunity. @dylanhmorris wrote a great article on this that is *highly* worth a read: theinsight.org/p/novelty-mean…
but to expand a bit: once we have immunity to a virus, generally* the virus stops being able to cause *disease*. in some cases, immunity is more-or-less sterilizing, i.e. you *generally* don't get symptomatic disease.
*yes i know about Dengue. ADE has not been observed here.
i was prepared for some potential bad takes when i opened nature.com/articles/d4158… but last 2 paragraphs just blew me the fuck away.
let's start with, uh, how little empathy do you have to have to write the words "more death, although seriously concerning, is a minor problem..."?
anyway i seriously am blown away that this person is a virologist. i thought that we moved past the whole "partial immunity" nonsense an eternity ago.
you can select for escape mutants towards a monoclonal or an antiviral. b/c those can't fucking ADAPT to the virus.
guess what our adaptive immune system can do, OTOH? this is assuming it manages to escape a complex polyclonal response over multiple arms of the adaptive immune system.