Ok, lets examine this in order. I’m going to piece this together based on what I’ve gleaned from you guys so you’ll have to correct me if I misrepresent something.
But before that lets reiterate what SARS CoV-2 is not. It is not the result of passage or directed evolution of RaTG13, and cannot be derived from the so-called GoF work the WIV was doing with the TOOLS WE KNOW THEY HAD
In 2012 the miners get sick in Yunnan and 3 die of ARDS. The WIV theses suggest that they may have been infected with a bat CoV. Serology apparently suggests that they have Abs against bat CoV N protein.
There are 3 possibilities here. (1) They got sequence, (2) they got sequence and live virus, (3) they got neither. That sequence was either RaTG13 or an undisclosed proximal ancestor to SARS CoV-2. If it was RaTG13 at this point there is no case because it can't be made into CoV2
Whatever, something allegedly spooked them sufficiently to go high-tailing down to the mine to take samples. They come back with stuff – most likely bat swabs or tissue in RNAlater (i.e. dead but good for sequencing).
From that they maybe get RaTG13 and the other more distant viruses just released and that were the mysterious outgrouping in the thesis that were omitted from the 2017 PLOS Path paper. you have to invoke they found something else that they havn't disclosed – the proximal ancestor
Wherever they got this sequence and/or virus, at some point in the next few years they start working on it and growing it. This at some point infected a lab worker(s) who then seeded outbreaks almost simultaneously at markets with different lineages of CoV-2.
OR they further made a molecular clone of this virus and then engineered it via passage in human cells and hACE2 transgenic mice, including inserting an FCS (suboptimal with codons you wouldn’t use if you were smart).
Again, at this point workers at the WIV got infected and seeded Wuhan as above.
So this whole thing hinges on the presence of this mythical ancestral virus. If they didn’t have it, WIV cannot be the origin of SARS CoV-2 no matter what else they were doing, what containment they used, or what KGA wrote in an email
Most likely vectors would be a member of the Zhi lab – but they’re all seronegative according to them. According to unsubstantiated intelligence, 3 WIV workers are reported ill. They visit the hospital – not uncommon I hear for Chinese to do this even with flu (and it was season)
Now given our unhappy experience here, and clearly in Wuhan in Dec/Jan, how do we account for there being no outbreak in the hospitals?
Lastly, most initial cases known are associated with one of 3 wet markets, and the known epidemiology shows the infections moving from there west across the river – ie towards the WIV not away from it.
So that’s a huge operation of lies upon lies, and fabrication, and the absolute requirement of a hitherto unidentified proximal ancestor virus for the lab leak to have legs.
So let’s examine the zoonosis hypothesis. Bat sarbecoviruses are endemic in horseshoe bats in SE Asia. They circulate in many subspecies, and show such extensive recombination that for a lot of its genome, RaTG13 is not the closest relative of CoV-2.
Many of these viruses can use a promiscuous array of mammalian ACE2 orthologues to get into cells. Some, like the virus identified as a zoonotic infection of pangolins have an RBD much closer to CoV-2.
Importantly, these viruses can infect species we know to have been farmed in Yunnan, a province where (an albeit small sample) suggests that around 5% of agricultural workers are seropositive.
And we know that such live susceptible animals from Yunnan and elsewhere in China were on sale in the markets that were the initial foci of the outbreak.
So a very plausible route is either spillover at the farm and propagation in animals that then went to market, or infected farmhands driving their wares to on a truck Wuhan.
Now what about the FCS? It’s not natural. Well, it certainly is in other lineages of beta-CoVs like MERS and HKU.1. We have only the tip of the iceberg in the diversity of the sarbecoviruses in SE Asia, and to suggest that this isn’t something out there in the family is foolhardy
So that’s in essence how I understand the 2 competing hypotheses. One hinges on something very specific being true for which there is no evidence at present followed by a bunch of tenuous circumstantial evidence which we cannot rule out.
The other a wealth of natural history about a family of viruses we are only beginning to understand, for which (due to Chinese negligence) we have a plausible route to Wuhan.

Now tell me gain why the former is more probable?

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More from @stuartjdneil

23 May
So may as well add my 2pth-worth

The data PHE released yesterday alongside other data suggesting B.1.617.2 is outcompeting other variants in India makes a good case for this virus having enhanced transmissibility compared to B.1.1.7.
No evidence yet of enhanced pathogenesis either, but these data will take longer to accumulate.
This may well be in part due to changes in spike, BUT, as for B.1.1.7, it is not yet clear if variations in other parts of the genome play a role in relative transmission differences. And I doubt immune-evasion explains transmissibility
Read 14 tweets
20 May
So this is an interesting thread, but there is nothing new here that adds any further evidence

1: they sequenced a bunch of bat CoVs from the cave by taking bat shit or anal swabs - probably into RNA later. these sequences should be published but, seems they were partial.
They used the WIV1 backbone to do the experiments that they published in PLOS which in pains me to reiterate CANNOT be the source of SARS2 itself
And lastly analyzed blood samples of the miners for antibodies to CoVs.
Read 4 tweets
20 Jan
With is manuscript from ⁦@PaulBieniasz⁩ and co, that from ⁦@RealMcCoyLab this AM⁩, data from ⁦@10queues⁩ yesterday and the prelim data from South Africa,

The variants we are seeinv have evolved to escape antibody.
biorxiv.org/content/10.110…
How and where to be determined.

Thus far it’s a mixed bag about how much they are resistant to serum from wave 1, and vaccinee serum while slightly reduced in potency, still works. (Good news!)
But these mutations, partic 501Y (Uk, Sa and Brazil) and 484K (SA and Brazil) do completely abolish the activity of some specific individual RBD antibodies.

More alarmingly the SA variant is insensitive to about half of wave 1 sera tested.
Read 8 tweets
1 Jan
I am becoming deeply troubled over the cavalier way the UK vaccine roll out is being changed on the hoof.

We have 2 approved vaccines that work to induce protective immunity.

They are both safe

I understand the haste to get them into as many people as possible.
But the phase iii data doesn’t exist to support their use in combination.

They are not quite the same immunogen. So homologous and heterologous boosting may accentuate different responses. And it might matter which order.

We do not know anything about this.
Next the timing

AZ boosting at 3 months turns out to boost higher Ab levels - another ‘serendipitous’ thing to fall out of the trial. Fine. But how protective is one shot?

And changing the Pfizer regimen, based reanalyzing the data to look for an answer they want. Probably true
Read 5 tweets
23 Nov 20
We need a good hard look at the numbers and the longevity before we conclude that this is less effective than the mRNA based ones. bbc.co.uk/news/health-55…
Firstly it seems to rise to 90% when the first priming dose is lower. This might mean that less is more, and potentially anti-adeno responses might limit the boost. If so this is serendipitous as it will halve the cost of production of round 1
Secondly, in this trial they have evidence of reduced assymptomatic infection in vaccinees, suggestive of less transmission. This is something that we don’t know for the other vaccines thus far.
Read 7 tweets
19 Sep 20
There a lot of scientists in reflective mood as we face up the prospect of an autumn second wave of SARS CoV2 and what it may or may not mean, and in particular whether we can or even should contemplate further lockdowns. So I’ll add my twopenneth’ 1/n
At the beginning we didn’t heed the warnings from China and Italy until it was too late and we ended up playing catch up with a rapidly spreading virus that we didn’t understand. 2/n
The ability to test samples and act on that knowledge was rapidly outstripped by resources and the govt were woefully slow to alleviate bottlenecks in testing, diagnostics and PPE, all of which had been highlighted when wargaming a pandemic 2 years earlier. 3/n
Read 27 tweets

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