Thread by @ClaireBerlinski

I would like to hear from any qualified #virologist who could tell me if this essay strikes him or her as unconvincing in its outline or its particulars, and why, precisely. It seems to me as close to conclusive as we can be absent direct evidence--

https://twitter.com/ClaireBerlinski/status/1390411766321061893

but I am not a virologist, nor even a biologist; surely there are aspects of this I don't understand. Nonetheless, here are the points he makes that strike me as compelling, and my specific questions about them:

1) The statement in the Lancet was organized by Daszak, who did indeed have a conflict of interest. That alone wouldn't especially strongly bother me--it's a fallacy to assume the statement wasn't correct because of that. But this does:

Wade is right to say they could not possibly have asserted what they did, with such confidence, at that stage. They cited a host of articles that in reality said little that suggests this kind of confidence.

For example, they cite this article, which actually says nothing of the sort: onlinelibrary.wiley.com/doi/full/10.10…. "Originated in bats" does *not* preclude "introduced to humans through of gain-of-function research gone awry in a lab." (Hereinafter, GOFRGAIAL)

And this one, sciencedirect.com/science/articl…, which rejects "a recent recombination event." I don't have access to the full paper, so I'm missing the whole argument, but the abstract's conclusions don't seem incompatible with GOFRGAIAL to me:

They are persuaded its origins are in RaTG13. Fine, so am I. But this would be perfectly compatible with GOFRGAIAL, is that correct?

2. Wade argues: "newer methods, called “no-see-um” or “seamless” approaches, leave no defining marks. Nor do ... serial passage." I'll take his word. But here's something else that strikes me: In the literature--you tell me whether it's worth reading--I've found this explanation:

nature.com/articles/s4156…
NB: "The SARS-CoV-2/RaTG13 common ancestor forms a clade of bat sarbecoviruses with generalist properties—with respect to their ability to infect a range of mammalian cells—that facilitated its jump to humans and may do so again."

IOW, they agree there's a clade of bat sarbecoviruses that *could* jump to humans. But this offers no evidence about *how* it did so.
(And their assumption that "the human ACE2-compatible RBD was very likely to have been present in a bat sarbecovirus lineage" seems to be based--

on the presumption of a common ancestor, which they *derived,* earlier in the paper, from the fact that SARS-CoV-2, RaTG13 and Pangolin Guangdong 2019 share ACE2-specific residues. Am I missing something, or is that an exercise in begging the question?

If you're looking at something and asking, "Hmm. How did this ACE-2 compatible RBD get here? Let's see if we can find other viruses that have it. Yes! We can! Okay, that means they all have a common ancestor,"

Well, *of course* you'll conclude it didn't get there because a lab put it there. But that's because you've just built common ancestry into your assumptions. Am I missing something?) But I digress. Point is, that we can plausibly imagine a biological process beginning in bats

and ending in humans, absent any human manipulation, is not *evidence* that this actually happened, particularly given that one way we manipulate viruses in the lab is by giving Darwinian mechanisms a boost, as in the serial passage technique.

I understand this, crudely, as akin to dog breeding. Yes, you *could* see a Best-of-Show French Poodle descend naturally from a couple of mutts. All the genetic ingredients, sure. Common ancestor, sure. But it helps if you've got breeders applying heavy selection pressure, no?

Anyway. I'm still open-minded at this point, but then we get to the arguments that really seem to me important.

3. SARS1 and MERS? Traces all over the natural environment. Intermediary hosts identified in months.

Wade writes--is this true?--that despite looking *very* hard, we've not found a bat population infected with SARS-CoV-2, an intermediate species to which it jumped, or serological evidence that any Chinese population, including in Wuhan, was exposed before December 2019.

That seems rather bad news for the consensus theory, no? Even a single SARS-CoV-2-riddled bat in a distant cave would confirm it, but if Wade's right, we can't find a one. Is he? If so, this isn't looking good.

4. Then we have the well-known fact that the WIV was indeed conducting gain-of-function research--as they proudly explain in Nature: nature.com/articles/s4156…

Very notably, they remark that they couldn't get SHC014 and RsWIV1-CoV to bind human ACE2. Receptors all wrong, alas. "Therefore," they remark blandly, "we synthesized the SHC014 spike in the context of the replication-competent, mouse-adapted SARS-CoV backbone."

Now, I am not saying that we have evidence beyond a reasonable doubt here that in so doing, they burnt down the world, but truly:

WHAT THE FUCK WERE THEY THINKING?!

Even if this was not the source of the pandemic, how could *anyone* be allowed to do this?

How could we have *funded* this research? Does anyone think it's a good idea to see if we can make viruses more lethal to humans just for the sake of seeing whether it can be done in a lab?

And does anyone think this kind of research should be done in a lab notorious for its poor biosafety practices--the State Department complained of it--and funded by the US taxpayer? They continue, blandly:

After conducting their experiment, "we examined the sensitivity of the human epithelial airway cell line Calu-3 2B4 to infection and found robust SHC014-MA15 replication." Great job, Frankenstein! Bravo!

And check out this paragraph. Do you understand what it says? (I am not asking virologists, now. I know you do.) I am asking people who may not quite get it. (to be continued.)

It says, "Something like this *could* happen in nature! That's why we need more funding! And we believe this because we *did* make it happen in a lab, using methods that are just like nature--

"except, of course, in one important way: we built a chimeric virus encoding a novel, zoonotic CoV spike protein, using the RsSHC014-CoV sequence from a bat. Other than that, just like nature."

Jesus fucking Christ.

But it continues. Please virologists, tell me if I'm misunderstanding this. I'm just a layman here. But this is looking rather bad for your discipline.

I've not yet even got to the most compelling part of the article. At least, in this layman's view. I'm really hoping someone out there who knows more than I do can set me straight if I've misunderstood, or if Wade has misunderstood: I do not wish to misinform people.

5. Shi returned to her lab in Wuhan to continue this work--and was *funded* in doing so by the National Institute of Allergy and Infectious Diseases, part of the NIH, so we actually know--no conspiracy theory necessary!--what she was doing.

Because we have the grant proposal. And yes, Wade is quite right to say journalists have not fully done their jobs here, isn't he. This should have been a source of more than passing curiosity, shouldn't it?

So, to repeat: Shi applied for a grant to see if it was possible to make bat coronaviruses as contagious to humans as scientifically possible. The scientific justification for this was that if we knew it was possible--

--perhaps we could do something about it before a pandemic just like this one emerged.

Revert now to the consensus idea: The pandemic just emerged without human help. Did this research help in any way to prevent this? Clearly not.

Might this research instead have *caused* it?

By the time I'm finished, you'll be wondering, too. Unless I'm misunderstanding everything. Always possible. I'm not a biologist, no less a virologist.

But as Wade writes, this isn't a conspiracy theory. It's an obvious hypothesis--and one that grows more plausible as time elapses and no evidence for the consensus hypothesis is found.

And Wade is right: That Daszak’s reaction to the news from Wuhan was to say, “The idea that this virus escaped from a lab is just pure baloney" is either evidence of a man involved in deep denial or a deliberate cover-up--

because he knew better than anyone what exactly they'd been cooking up in that lab, and *every* working scientist will confirm--please confirm, if you're a working scientist--"accidents happen."

(If you work in a lab, especially, please take this opportunity to recount your favorite hair-raising anecdote.) But this lab, in particular, was the last place such research should have been done. The State Department warned of this explicitly:

Two cables. The first warned the lab’s work created a risk of a new SARS-like pandemic. The second noted "a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory." washingtonpost.com/opinions/2020/…

Shi herself said the research was "conducted in BSL-2 or BSL-3 laboratories.” If you're dealing with a deadly pathogen, BSL-4 is the standard. This is what BSL-2 means: consteril.com/biosafety-leve…

In other words, BSL-2 is roughly what the home of every human being on the planet has looked like for the past 14 months, and clearly, that isn't safe enough, because three million of us are dead. (I still haven't got to the most important parts.)