Yes the virus emerged in Wuhan & the WIV is there & studies SARS-related CoVs, but that’s where the truth ends.
Shi Zhengli’s lab does great work on SARSr-CoVs, but they aren’t the only lab in the world doing so. They aren’t even the only lab in China doing this work.
In fact, people all over the world have been studying these viruses—including those isolated from bats—since SARS1 emerged in 2002. In the US, Australia, Hong Kong, Singapore, the UK, the Netherlands, Japan, France, Canada, and so on.
Fun fact: early in 2020 I joined a WHO Expert Group on experimentally modeling SARS-CoV-2. Multiple folks from China were there, none of whom were from WIV or Wuhan. SARS-CoV-1 emerged in China, so many labs there study these viruses. Wuhan isn’t special & WIV is one of many.
This is a little confusing, since the “defining feature” isn’t actually defined by the author. But she means the furin cleavage site.
She also neglects to mention this proposed work was not funded (thus likely didn’t occur) & all the FCS insertion work was to occur in the US.
And could this work have been done despite the multimillion dollar grant intended to support it? Sure. Is there evidence that this work was carried out anyway?
None whatsoever.
Most people don’t apply for DARPA grants they don’t need if they already have millions lying around
Yes the WIV did SARSr-CoV work at BSL-2 (consistent with the BMBL, the US’s standards for bat SARSr-CoVs).
No, this isn’t appropriate for SARS-CoV-2.
However, there is zero evidence that WIV had SARS-CoV-2 or a progenitor in their collection.
No SARS2 at WIV, no lab leak.
That’s pretty simple. It doesn’t matter what containment level the WIV was using for other SARSr-CoVs because those viruses are not SARS-CoV-2, nor could these viruses ever become SARS-CoV-2.
The viruses that WIV was known to have are more closely related to SARS-CoV-1.
Even the most closely related SARSr-CoV (RaTG13) in WIV’s collection is different by more than 1100 mutations across its entire genome. No amount of insertions, mutagenesis, or passaging in cells, transgenic mice, bats, or whatever else can make it SARS-CoV-2.
I’m closely related to my sibling and my parents. If I got cancer or HIV (which would cause mutations/insertions/recombination of my genome), it would not turn me into my brother or my parents.
Similarly, the WIV’s SARSr-CoVs can’t turn into SARS-CoV-2 at any containment level.
This is just plain incorrect. The hypothesis was published with enough supporting evidence to pass a rigorous peer review and be published in Science. The papers have not been retracted.
And just because a small but outspoken group of people—primarily those without any relevant professional or domain expertise, including the author of the NYT piece—claim these papers are disputed, debunked, or aren’t “strong” evidence doesn’t make those claims true.
If anyone can provide a legitimate analysis or plausible alternative explanation for these multiple threads of evidence, then they should submit it for peer review by experts and publish it in a scientific journal.
So far no such paper has been produced.
Here’s a summary of the Worobey et al 2022 paper.
Critics have had 2 years to challenge these results scientifically, providing additional evidence or a compelling alternative interpretation of these data. These papers & their findings have not been substantively challenged.
Finally, no shit “key evidence” is still missing. The role of the market in the pandemic’s emergence was covered up in ways that didn’t apply to SARS1 or MERS. The market was closed. Live animals were removed. Clearly evidence was suppressed, not collected, or not made accessible
However, that doesn’t mean the evidence we DO have doesn’t support market origin. Existing affirmative evidence isn’t invalidated by a lack of other types of evidence.
Again, I have yet to see an alternative explanation for the multiple threads of evidence supporting zoonosis.
“No infected animals at the market” (because samples weren’t taken to look for said infected animals) doesn’t disprove all the other evidence that very clearly points to the market.
Evidence isn’t a carton of milk. It doesn’t expire if you don’t find it. Intermediate hosts of SARS1 and MERS were not found in days as claimed and sometimes they are never found. It took years to find the reservoir for Marburg virus. Nobody debates that it is zoonotic.
Supposedly this was fact-checked by @nytimes—not well enough.
This matters. Watch this clip of Dr. Fauci talking about the sickening threats made against him & his family.
Factually incorrect claims like those in this piece encourage these threats. cnn.com/2024/06/03/pol…
It is grossly irresponsible to say that these 5 unsupported claims mean the pandemic “probably” started with a lab leak. They misrepresent the actual evidence and put people like Dr. Fauci at great risk.
The @nytopinion has shamed itself by printing untruths & outright lies.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
My replies are perpetually full of anti-vaxxers these days telling me about polio vaccines.
Not shockingly, most of what they are saying is wrong. Luckily, I trained with @profvrr & he taught me a few things about poliovirus.
So let’s discuss the king of the Picornaviridae👇🏻
Let me start off by saying that while poliomyelitis is a terrible disease & I am anti-polio, I fucking LOVE working with poliovirus. It routinely grows to titers of 10e9 in HeLa cells & makes the clearest, most beautiful plaques even in BactoAgar that every other virus hates
Because poliovirus infects via the oral-fecal route, it can tolerate highly acidic environments like the stomach. It’s non-enveloped and virions are highly stable across a wide range of temperature & pH. You can leave PV at room temp for days with minimal reduction in titer.
In terms of basic technical requirements, H5N1 cannot become a pandemic virus without adapting to its host. For humans, that means adapting to different receptors, body temperature, host cell types, tissue organization, etc etc. Big changes from the avian host it’s adapted to.
There are multiple barriers a virus has to overcome to replicate in a new host: 1. Entry (and often fusion)-viruses can’t infect cells they can’t get into 2. Transcription/genome replication-gotta express viral genes and copy the genome to package inside progeny virions
Thanks to the first Canada acquired H5N1 case, there’s an uptick in “bird flu pandemic imminent” and “omg it’s gone H2H!” posts. Those are not accurate.
However, given the situation in the US, I have some real concerns about this that grow progressively more grave.
First let’s get this out of the way: while a case has never occurred locally in Canada, there have been many human cases of H5N1 during this panzootic (since 2021).
It’s probably direct spillover from a bird or other animal, not human to human transmission.
But as we’ve seen in the US with dairy and poultry workers, spillover to humans will occur if there are opportunities for exposure. Right now in the US, there are many opportunities for exposure in both the dairy and poultry industries.
Finally, we have H5N1 serology data from Missouri. 🙏🏻 @CDCgov.
Both the MO patient and their household contact were positive for antibodies against H5N1 in 1/3 tests. This is not definitive per WHO criteria (2 tests positive) but does suggest infection.
Testing positive on just 1/3 tests may suggest that these patients had a transient infection. Weak seropositivity can indicate low titers of antibodies, consistent with an immune response to low levels of virus replication.
That’s good news. A more human-adapted virus would be more fit, replicating more efficiently, producing more virus, and increasing the chances of onward transmission.
This suggests that this virus isn’t very fit in a human host.
A question I have concerns the animal host. Was it R. aegyptiacus (known Marburg reservoir) or something else?
Because this “limited mutation rate” is interesting. Ebola (also a filovirus) appears to persist without replicating much as seen in outbreaks in survivors.
And if this “limited mutation rate” suggests few mutations compared to the 2014 virus (would have to actually see the data), it might indicate something similar is going on with Marburg too. Potentially in an animal host, since there haven’t been human cases in Rwanda before now.
Ebola pathogenesis is brutal and super complex. When people hear Ebola hemorrhagic fever (now Ebola virus disease or EVD), they shouldn't think Ebola kills cells and causes bleeding. They should instead think Ebola causes a massive, uncontrolled systemic inflammatory response.
A brief description of Ebola pathogenesis: 1. Infect macrophages & DCs in peripheral tissue 2. Infected cells go to nearest lymph node 3. Repeat 1 + kill B & T cells. Viremia ensues 4. Dump proinflammatory cytokines into bloodstream & you get intravascular coagulation