I don’t have anything to add to this beyond the videos posted at the top, so instead, I’ll just recommend the two recent episodes on this topic from the If Books Could Kill podcast:
If nothing else, I want to direct everyone the short segment from the second episode, from 1 hour 3 minutes and 50 seconds to 1 hour 5 minutes and 30 seconds. Listen to that. I cosign that whole bit.
It is not even close.
That’s not remotely equivalent to what @Jon-Perry wrote.
The truth is that the evidence for a zoonotic origin of sars2 that should have been easy to collect if the theory was true are cruelly lacking and this is highly significant.
The Absent Evidence is Evidence Against Zoonotic Origin
The absence of evidence for a zoonotic origin is significant in and of itself. We lack a geographic trail of infections. We lack evidence of animal traders having a higher incidence or PCR-positive environmental samples compared to vegetable traders. We lack a reservoir in Wuhan with a SARS CoV despite extreme sampling, and in fact we lack a single documented case of a furin cleavage site in a SARS-CoV outside of SARS-CoV-2. While a spatial analysis of early outbreak cases provided by the Chinese government centers around either the Huanan seafood market or the Wuhan CDC, the Chinese government has not released the one database of pre-COVID coronaviruses under study in Wuhan that could, under a zoonotic origin, exonerate their labs.
So the complaint is that we lack a time machine. Better start working on that flux capacitor.
Oh great, Alex Wasburne again. His preprint paper (still not published) was just awfull, and we went over this in detail years ago. You were there too.
Of exactly what? Geographical clustering of early cases? Then this is false. The Huanan Seafood Wholesale Market in Wuhan was the early epicenter of the COVID-19 pandemic.
Even if we were to do this right at the time of the outbreak, this wouldn’t do much good either since MOST animal traders and their stuff would be tested negative too. You would only do this if you expected that most animals (of the suspected species) that are traded would be infected with the virus you are looking for, but this would not be the case.
What you would do is testing suspected individuals at the location of the outbreak. This is how they identified infected palm civets at a wet market within 4 months after the SARS1 outbreak in 2003. But they were able to do this since the market continued to operate like normal, selling living animals. This is different from our situation where the Chinese Government promptly shut down and sanitized the wet market, with all the animals were culled and disposed (except for a few frozen animals). This is similarly true for all the wildlife farms nearby. It’s thus not surprising that we did not find a living animal infected with SARS2. (See discussion by Paull Offit for more). And SARS2 is not alone in this regard too. The animal origins of Ebola, Hepatitis C, Polio, and even other human coronaviruses (HCoV-HKU1 and HCoV-NL63) are not identified (see discussion here). It also took 14 years after SARS1 outbreak to identify reservoirs in bat populations with >95% similar viruses. In short, next to no animals were available to test. Hence ‘absence of evidence ≠ evidence against’ in this case.
Having said that, we do have environmental samples from the wet market. Some studies that discuss this include here and here.
The reservoir is not necessarily at the location of the outbreak. Again, this is also true for SARS1 as well as SARS2. Both reservoirs are located over a thousand kilometers away from the sites of their respective outbreaks. Details discussed in this recent paper.
Ah, an old argument. While not found among the closest relatives of SARS2, Furin cleavage sites are nonetheless found among betacoronaviruses, and have evolved multiple times within this group. This also includes those that cause the common cold in us, such as HCoV-HKU1 for which (as previously mentioned) we have not identified the animal source. Humans are the only known reservoir of HCoV-HKU1. So it’s not out of the question that SARS2 could’ve evolved an FCS as well. (For more see here, here, here, and here)
I think that sentence does matches the broad strokes of the DEFUSE project outline, minus the details, but can you explain what you mean exactly why it doesn’t match?
Because you described sequencing particular things (typically amplified by RT-PCR) and Jon did not.
It is.
What anyone says about the evidence isn’t the evidence.
Well… Jon actually did say “sequence”, even in the part hat you quoted (see highlighted)