1/7:
Last week at the European Congress of Virology in Gdansk #ECV2023 I deep-sixed the raccoon dog market theory of #Covidorigins by questioning Martin Beer, senior author about their key paper (Freuling et al. 2020)
2/7 I asked why they tested a more transmissible G614 strain and not the original D614 strain, which would have supported or eliminated raccoon dogs as a potential intermediate host.
His answer was not "thanks, good idea we'll jump to it". He stumbled a bit and then, incredibly.
He said: I paraphrase slightly: "he didnt know whether D614 or G614 came first"
This is an astonishing answer on many levels.
Absolutely no one thinks that D614 came after G614. Because: 1) D614 was detected first 2) G614 displaced D614 as the pandemic progressed 3) See below...
4/7 3) G614 outcompetes D614 in all known animals and cells, 4) D614 is found in RaTG13 and BANAL-52, the ancestors.
And since, as Prof Beer knows FROM HIS OWN EXPERIMENTS that G614 transmits between ferrets while D614, the original strain does not, this rather suggests....
5/7....that testing a D614 strain on raccoon dogs would show they cannot transmit origin strains, thus torpedoing the raccoon dog theory and hence the market origin. Thus he knows, and I know, and the audience at #ECV2023 now knows and shortly twitter will know, that Prof. Beer..
6/7 and his colleagues are well aware that raccoon dogs would not transmit origin strains. They are therefore shamelessly protecting the raccoon dog theory and thus the zoonotic origin of #SARSCoV2 from collapse.
Or maybe, worse, they did the experiment, and they already know,..
7/7 but have chosen not to communicate the results.
1/few. Attendees of #Nido2023 may be wondering why I am not being allowed to ask questions of the speakers. Attendees should know too that I was denied the right to share our printed scientific articles. No reason given so far except the "instructions of @ProfVolkerThiel" ...
3/few.
questions, thus exposing his research program as not a fair-minded and objective enquiry into #Covidorigins but a veiled defence of the zoonotic origin.
Here is a link to our discussion:
1/3 My experience of #Nido2023 (the coronavirus meeting in Montreux) so far 1) The organisers refused to let me share the materials I bought. That is, two articles, one on #Ebola2014 and our proposed origin of SARS-CoV-2
This is under the instruction of Swiss virologist Volker Thiel.
They have also been removing ones I have left around while I have been attending the talks. T
They also stopped me asking my question to ZLS.
See next tweet below:
At the conclusion of Shi Zhengli's talk the microphone person went over to hand me the microphone but the podium stopped them and sent them to another questioner.
Then I put my hand up again and a different microphone person came over to me....
2) The orthodox origin story has negligible evidence to support it. No #Ebola was found at Meliandou, Guinea, or elsewhere in wild animals nor was it diagnosed or positively tested in 'patient zero' or his contacts. The nearest known wild source was a whopping 3,000 km away
3) The subsequent epidemiological investigation back from the first confirmed cases was also highly speculative. E.g. the father and others disagree that his family had #Ebola, even tho' the epidemiology was supposedly largely based on interviews. #Ebola2014
Wanted to try a twitter tutorial (our first, so bear with it) on the v. interesting #CRISPR issues raised by the recent birth of #geneedited#Calf "Cosmo", thx to @UCDavis researcher @BioBeef. Author @MeganMolteni gamely brought in some perspective but no technical critic, so....
The following are issues neglected or barely raised in the text but should be born in mind while reading the article, which described attempts to add the SRY sex "determining" gene and make all male animals: wired.com/story/a-crispr…
2 The researchers began w/a "crude portrait" #genome sequence (so the first embryos died because the researchers chose the wrong place to edit). The premise of #geneediting is precision but this requires EXACT knowledge of the target genome, which almost invariably is lacking.