5) "Research on the cross-species infection and pathogenicity of bat viruses" this is literally directly related to the southern Chinese bat CoV hACE2 survey grant I continue to link, which you continue to ignore
6) more stuff about a grad student I never mentioned and consider obviously uninvolved
7) nothing whatsoever in my argument is based on Chinese social media rumors or similar, but rather entirely on papers, manuscripts, and I suppose maps
8) if a researcher was infected, it would have likely been a mild case, but either way it is irrelevant whether or not the first infected individuals died
9) I agree: the distinction between infection by a stored undisclosed natural strain vs. recombinant is irrelevant
11) I have said nothing about animal escape, which seems if anything less likely than an unnoticed accidental human infection given long contagious incubation period
12) again you claim diversity of arguments is a weakness
17) "scientists could have replaced the RBD of a bat coronavirus related to RaTG13-CoV... which might have given rise to SARS-CoV-2 either directly or after enough rounds of simulated evolution" they literally wrote about doing this
18) "Again, this is certainly possible, but lots of things are possible and most of them never happened" usually the ones declared in grant proposals do actually happen, otherwise it is called fraud
19) "If you want to blame China" something similar could have just as easily happened in another country-- the original H5N1 ferret gain-of-function study was done in the west, and the U.S. moratorium on gain-of-function work had expired. China merely discloses less.
21) "it raises the probability that SARS-CoV-2 was bioengineered at the WIV somewhat, but the fact that I’m a man also raises the probability that I’m a serial killer (since they are more often male)"
A better analogy: being the only known male within 1900 km
22) "bat coronaviruses are massively undersampled," I agree, but bat coronaviruses are carried by bats-- which hibernate or migrate in winter. Wuhan is not even within the northern or southern ranges of horseshoe bats, and SARS-CoV-2 solely resembles southern strains.
24) "However, had they used RaTG13-CoV as a backbone and simulated natural selection to create SARS-CoV-2 in that way, there would be signs in the genome of the virus that it had recently been under strong selection" I agree, which is why the recombinant study fits best
25) "they almost certainly didn’t use RaTG13-CoV but another bat coronavirus nobody except them knows about. I guess it’s possible, but there is no reason to think it ever happened."
Again, except for a grant describing doing exactly this.
26) "If researchers at the WIV had been doing that kind of experiments, it’s surprising that no scientists elsewhere had heard about it through the grapevine"
27) "Only someone who is already committed to the lab escape theory would have a reason to make this hypothesis, because otherwise this version of the theory is untenable"
I became most concerned about it when I saw these papers and then this grant, actually.
28) "But there was no reason to think this RBD should have been good at binding human ACE2 and, on the contrary, structural analyses would apparently have predicted it wasn’t optimal at doing so." The grant discusses direct in vitro assays to find RBDs that bind hACE2.
29) after this, you make more arguments centered on WIV dutifully uploading all of its sequences to public databases, which is ridiculous given they didn't even upload the ones from the infected miners years ago
30) "The same thing can be said about the version of the lab escape theory according to which SARS-CoV-2 evolved naturally, but ended up in a lab where it was studied by scientists and from which it accidentally escaped" that does not need sequencing, only mishandling
31) "we can’t rule this possibility out (... viruses have escaped from labs before), but we also have no reason to think it actually happened." Except for being the only known source of extremely closely related viruses within 1900 km, and actively infecting animals
32) "We’d have to assume that scientists at the WIV had discovered... another, closely related virus that somehow infected someone at the lab or in the vicinity, circulated in humans"
That literally happened, ironically, but it is not required.
34) yes, there were known safety issues at WIV, but that isn't even the point-- SARS-CoV-2 is highly transmissible, including though aerosols, and there are many documented instances of workers in BSL3/4 labs in many countries being inadvertently infected by pathogens
35) "this passage is more naturally interpreted as saying that the work in question was important to prevent the emergence of another coronavirus that can transmit to humans"
this has always been the fig leaf for gain-of-function work
36) "the controversial experiment was performed at the University of North Carolina, not the WIV" in 2015, by people who left for China when the U.S. imposed a moratorium on gain-of-function research funding, including e.g. Zheng-Li Shi.
37) you note the Wuhan Center for Disease Control and Prevention is located only a few hundred meters from the Huanan market-- this is very interesting, as it provides further reason for WIV staff to visit the area
38) I am not proposing a particular stochastic model
Note I interpreted some of the events a bit differently. I say 'lab' if it starts from a lab anywhere in China. I say 'not lab' otherwise. I say 'Wuhan' if it starts in Wuhan, 'not Wuhan' if it were to hypothetically start in another city instead.
Given the wide range of different results obtained from this model, I would argue that it is rather useless in this form for drawing a conclusion in its own right-- serving more as a mere sanity check for a hypothesis.
...
@phl43@YmeKindsome@antihero_kate "shouldn’t fool ourselves into thinking that we’re going to prove or... refute that SARS-CoV-2 escaped from a lab with this kind of mathematical tricks."
Agreed.
"have the appearance of rigor, but they are really tools of persuasion"
This is largely due to poor ACE2 affinity, absence of furin site, etc.
The obvious conclusion is that optimizing hACE2 binding as the grant describes makes it more likely to have been artificial.
@phl43@YmeKindsome@antihero_kate I do not expect you to bother updating for new evidence or to even read any of this. I will be surprised if you do.
I wrote this to check for myself-- as to whether there is anything important that I might be missing, as you seemed very convinced above.
@phl43@YmeKindsome@antihero_kate I conclude there is not, or at least not in this essay. You are simply missing key evidence-- the same evidence that caused me to reconsider my earlier view, which was previously more similar to yours.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
- decide what the word "evidence" means:
a) "clinical results with appropriate sample(s) and endpoints"
b) "what huge lumbering institutions claim ex cathedra with no citations"
c) "what gilead et al. claim"
d) "peer best practices"
- take low-risk bets
If in doubt, *ask the patient*.
People have a fundamental right to participate in their own health-- *they already do so 99% of the time anyway*.
'This might help with X; it's a bit less certain; may cause Y side effects; studies say usually well-tolerated; do you want to try?'
The continued failure to trial or use ITPP in critical care is an indictment against the regulatory and productive institutions of our supposedly-advanced (increasingly just shorthand for 'gridlocked') economy.
Thousands of people already use it for athletic activities.
It has no side effects, is safe at huge doses in animal studies, and has never had a serious adverse event reported in the community ('that's informal' it's post-marketing surveillance..).
The fact that we are jamming tubes down people's throats before giving this, or for that matter even giving cyproheptadine, absolutely disgusts and appalls me.
>Oh that isn't proven
Yes. It. Is.
READ A BOOK; THEY ARE BOTH LITERALLY BASIC PHYSIOLOGY.
>One hope is that the efficacy of the Johnson & Johnson vaccine could rise if it is given as a two-dose regimen.
Obviously, yes! This is much more promising.
Single-dose frankly seems gimmicky, in a very specific sense:
This is effectively just offloading the debate about whether to halfway-dose existing vaccines to a new vaccine candidate instead-- one that has actually been trialed in this dosing schedule.
A couple things about which I would like to be clear, from the now-big account (likely smaller over time):
1) do not ever @/DM to ask where I am or act like I owe you something-- pay me a bitcoin if you want that kind of attention, I know that is pocket change to some of you
2) I have a life outside of COVID-19 and a very, very detailed post history that is approximately two clicks away, depending on your choice of platform access method: search feature, "__ice9 <whatever topic>" papers generally do not become 'out of date' and a result is a result
3) I am frankly a bit bored. The acute disease was obviated months ago by dual entry inhibition. Not my problem if the west ignored it because it came from Iran, or due to statistical illiteracy or vile conflicts of interest (hi Gilead puppets 🎭). Fluvoxamine looks great too.
Side note: strangely demanding PK study; very rigorous protocol. Hope participants were at least paid well. But they got us a number so I am pleased.
NAC may not have a large impact in monotherapy, given only EC50 is hittable (not EC90 except perhaps IV) and gappiness in plasma concentration peaks even q.i.d. (slightly compensated by permanent nature of damage done to exposed Spike copies).