I feel I must reply to a comment from @DavidRelman in a recent @nytimes article on a piece of mine in @ScienceMagazine on why a careful analysis of the earliest known cases in Wuhan indicate that the pandemic started at the Huanan Market.
“It is based on fragmentary information and to a large degree, hearsay,” David A. Relman, a professor of microbiology at Stanford University, said... “In general, there is no way of verifying much of what he describes, and then concludes.”
Here is the article, for those who would like to test David's dismissals against what I actually present in the piece. I do hope you'll do so.
I am concerned about anti-scientific comments like this that reflect a desire to downplay, denigrate, or dismiss evidence that doesn't suit the desires of advocates of a particular hypothesis (in David's case, the lab leak hypothesis).
There is enough of this sort of "I'll-believe-what-I-want-to-believe-in-the-face-of-all-evidence-to-the-contrary" going around these days for it not to leak further into scientific discourse.
More concerning is a strain of bias, also present in other leading proponents of lab leak scenarios such as @Ayjchan, where first-hand comments by Chinese doctors, scientists and, apparently COVID-19 patients, are easily and dismissed as lies or, here, "hearsay".
The strength of my article is that it draws on firsthand accounts - including audio/video recordings - of doctors, hospital administrators and patients like Zhang Jixian, Xia Wenguang, Wei Guixian, Chen Honggang, Ai Fen and Yuan Yufeng.
To deride and dismiss the accounts of these individuals as hearsay is beyond disrespectful.
It begs the question, why?
Zhang Jixian, at Hubei Provincial Hospital of Integrated Chinese and Western Medicine, for example, single-handedly worked out on Dec 27 that this was likely a new viral disease, human to human transmissible, with asymptomatic (lack of) presentation.
Is her account of these discoveries, and the soon-to-follow insight that most cases in her hospital were workers at Huanan Market, hearsay?
Are the recorded voices of early patients like Chen Honggang and Wei Jixian not vivid and real enough to be counted by @DavidRelman as non-hearsay evidence?
“In general, there is no way of verifying much of what he describes, and then concludes.”
There is a way: it just involves not dismissing the voices of the frontline workers and COVID patients in Wuhan as dishonest or hopelessly unreliable in recounting their own experiences.
I have spent the last few months trying to poke holes in the hypothesis of a natural origin of SARS-CoV-2 by asking:
Was the apparent preponderance of early cases linked to Huanan Market real or just a mirage because that is where people were looking for cases?
This is a key question, because if the pattern is real, it is *very* hard to explain why we would observe it if the outbreak had not started at the market, in particular the western section where illegal wildlife like raccoon dogs was sold. It's about the size of a Home Depot.
2/ In 1987, FDA approved the first HIV antiviral, AZT. Hope quickly turned to despair though, because in patient after patient the virus quickly evolved to become resistant to AZT.
It wasn't until 1996 that the key breakthrough emerged.
3/ At a conference in Vancouver BC, researchers revealed that if patients were given "triple therapy", cocktails of drugs that attacked HIV in different ways, resistance could be averted.
1/ Medium thread on #SARSCoV2's furin cleavage site and a strikingly similar region in some of the new BANAL genomes from Lao, and in RmYN02 from China.
Seems worth trying to clear up the confusion of @ydeigin on this issue (even it means broadcasting my pic, below).
2/ The furin cleavage site of SC2 is the RRAR in the NSPRRAR stretch of amino acids in the alignment I'm holding up there. It is what makes the virus 'pop' in humans.
The BANAL viruses have NSPAAR. A couple other ones, including RmYN02, have NSPAAR or NSPVAR.
3/ So, having barely scratched the surface of the genetic diversity of these viruses in the wild, we've found several that are literally a *single* amino acid away from having a furin cleavage site.
1: I want to follow up the thread below with some additional clarification of why we hypothesize that there may be no real #SARSCoV2 genomes transitional between lineages A and B.
2: @daoyu15 has written a thread asserting that we "toss any genomes that don't fit your conclusions away". I'm afraid this is incorrect on multiple counts.
3: What we show is that many of the putatively transitional genomes bear obvious evidence of being artefacts - probably due to bioinformatic pipelines, rather than sequencing errors per se. (Issues like calling a site with poor coverage to be the base of a reference genome.)
3: To explain, let me introduce you to 'lineage A' and 'lineage B', aka 'clade II' and 'clade I', respectively, in this paper by Zhang et al. These lineages co-circulated in China during the early days of the pandemic, and they differ at two key sites.