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.
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This is great news, as more testing is urgently needed, but there are some caveats.
Wastewater data can be difficult to interpret. It can be especially difficult to identify the source and won’t catch anything not connected to municipal sewage systems (many farms are not).
Because there is no data indicating widespread human infection, spikes of H5 in wastewater could indicate dumping of infected milk, birds or other animals defecating into sewersheds, etc. Unlike other environmental samples, the host can be very difficult to identify.
Host sequences are completely disentangled in from viral sequences in wastewater, so there’s no way to figure out where a strong H5 signal is coming from with the WW sequences alone. If there’s an obvious source (affected dairy dumping tanks of milk) that might explain a spike.
Out now on @virological_org: preliminary report on the genomic epidemiology of H5N1 sequences in cattle. This complements the preprint @USDA put out yesterday.
There was a lot of data to work with, so it's split in two parts 👇🏼
1. There was a reassortment event shortly before the cattle outbreak.
Only segmented viruses like influenza can reassort. If 2 viruses infect the same host, they can shuffle their genome segments like 2 decks of cards
1. Reassortant viruses can acquire new features, including the ability to replicate efficiently in new host species. In this case, some of the segments were from the high path Eurasian panzootic H5N1 genotypes & some from low path North American genotypes emerging in late 2023.
Very important to note here that qPCR positives are not the same as "virus particles." It's much easier to detect viral RNA by qPCR than it is to detect infectious virus or intact virus particles (as the article correctly notes).
1. This suggests there are undetected herds shedding virus into the milk supply. Viral RNA does not materialize out of thin air—it is the product of a current or very recent viral infection.
No virus replicating in cows, no viral RNA in milk.
No viral RNA, no PCR positives.
1+. qPCR detects virus by amplifying small specific fragments of the viral genome. There's no indication that they pulled entire H5N1 genome sequences out of this, which would likely require signaling. Influenza is segmented, however, so no word on which segments they amplified.
Here is the article linked above and what it actually says: “The Texas Animal Health Commission said in an email that sick cats tested positive for the virus.”
There may be more cats affected but I did not find a single credible report of more than these 3 cats (for now). Also to be clear there is no evidence that it is “spreading rapidly” in mammals & sequence data suggests transmission from birds.
The only things created or crafted here are these grossly incorrect heaps of horseshit generated by @caitlintilley @DailyMail & @nypost.
This article and others like it are very misleading. This was not gain-of-function research, no matter how many loud non-experts say it is.
This article describes this recent preprint published on @biorxivpreprint. Briefly, scientists in Beijing cloned a pangolin SARS-related coronavirus they had isolated & infected human ACE2 transgenic mice with it. All the mice died.
Mice have ACE2 (the receptor that many SARSr-CoVs use to enter a cell) but it’s not similar enough to human to allow efficient entry of SARSr-CoVs that infect humans. So to study these viruses in mice, you need mice that express a human ACE2 transgene.
In this commentary, me and 77 of my colleagues argued that virology research is essential to pandemic preparedness. Biosafety is a cornerstone of virology research, but technical expertise is required for regulation that actually works & can’t be excluded from policy development.
All of the co-authors are US-funded virologists like me, who have technical expertise in experimental virology or vaccinology, or biosecurity and biosafety policy experts who agree that technical expertise is required to implement effective oversight.