If Covid turns out to be a lab escape (which is a big if), the nation or lab it happened in is just the proximate cause. Deeper responsibility would lie with the institutions and individuals that pushed it despite the risks. No one knows the answer to this (edit: I mean to whether covid escaped from a lab), but it's an open question that deserves credible investigation. Having the investigator be one of the principal funders of the research being investigated is such...bad optics, to put it nicely, that one wonders how anyone thought that would be ok.
[1] https://mbio.asm.org/content/3/5/e00360-12
[2] https://www.nytimes.com/2012/01/08/opinion/sunday/an-enginee...
[1]https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndr...
Guess who found the bat host? Shi Zhengli of the very WIV in question.
There are many videos and articles on this site about how SARS-2-CoV was not zoonotic. I don't necessarily blame China, but the funders of the research.
https://www.peakprosperity.com/more-evidence-covid-19-may-no...
So a very likely explanation is some low level employees grabbed some bats, got their suits and vehicles contaminated didn't clean things properly, drove down to the Wuhan laboratory, and rested in town spreading virus contaminated dust or if they were already sick, their virus filled respiration about.
No lab leak needed, just the regular practices when "Wuhan Institute of Virology in China sampled thousands of horseshoe bats in locations across the country", and those doing so were being sloppy, as they have been known to be repeatably.
[0] Bat cave solves mystery of deadly SARS virus — and suggests new outbreak could occur - December 2017 https://www.nature.com/articles/d41586-017-07766-9
But then, we should probably also apply Hanlon's razor [2] "never attribute to malice that which is adequately explained by stupidity"
This is untrue. I'd point to this quote:
“It’s pretty apparent that there’s this evolutionary arms race between the receptor binding domain and ACE2 that’s happening within the bats themselves,” says Tyler Starr, a postdoc in the lab of genome scientist Jesse Bloom at Fred Hutchinson Cancer Research Center. “Whatever it’s doing is ratcheting up this evolution and sometimes spitting out things that can bind potentially to many different ACE2s, including ours.”[1]
The unique thing about COVID is the transmission and the long incubation time.
There are plenty of naturally occurring mutations that have occurred that are more contagious than COVID (AIDS R0=~4.5, Ebola=~2.5 are two major ones that spring to mind). And SARS1 had a very similar binding behaviour, and the jumping behavior via civets is very similar to COVID.
[1] https://cen.acs.org/biological-chemistry/infectious-disease/...
Also, my understanding (quite possibly wrong) is that while humans can get sick from bats, as cave workers did in Southern China, those viruses aren't contagious in the sense that the sick humans go on to infect others. "Since no case of an epidemic caused by direct bat-to-human transmission has yet been demonstrated, it is thought that the transfer to humans more probably took place via an intermediate host species in which the virus could evolve and move towards forms likely to infect human cells." [1] If that's right then your explanation of spilled bat samples is incomplete: it doesn't explain what caused the bat samples to adapt into a form that could spread among humans. That sort of puts us back at square 1. Another way of saying this is that if your explanation is likely, then we'd have expected the pandemic to have started where the bats are - through sick cave workers or something similar. But in fact it started far away.
[1] https://news.cnrs.fr/articles/the-origin-of-sars-cov-2-is-be...
The leader of the Wuhan team went there with a team to collect samples and animals. In the early days of Covid, those samples were re-examined and it turned out that the genome of the Covid strain was very similar to the Covid 19 virus. So the conclusion was taken that those bats must have been the origin where Corona somehow started. Somehow nobody at that time thought much about the fact that those samples were kept in Wuhan, exactly where the outbreak started.
More than a year after the initial documented cases in Wuhan, the source of SARS-CoV-2 has yet to be identified, and the search for a direct or intermediate host in nature has been so far unsuccessful.
The low binding affinity of SARS-CoV-2 to bat ACE2 studied to date does not support Chiroptera as a direct zoonotic agent. Furthermore, the reliance on pangolin coronavirus receptor binding domain (RBD) similarity to SARS-CoV-2 as evidence for natural zoonotic spillover is flawed, as pangolins are unlikely to play a role in SARS-CoV-2′s origin and recombination is not supported by recent analysis.
At the same time, genomic analyses pointed out that SARS-CoV-2 exhibits multiple peculiar characteristics not found in other Sarbecoviruses.
A novel multibasic furin cleavage site (FCS) confers numerous pathogenetically advantageous capabilities, the existence of which is difficult to explain though natural evolution...
source: https://link.springer.com/article/10.1007/s10311-021-01211-0
https://news.cnrs.fr/articles/the-origin-of-sars-cov-2-is-be...
There are plenty of viruses from animals known to infect humans, viruses that have never been in humans and are not evolved to infect them, this happens alarmingly regularly. Here's a couple you've probably never heard of: https://en.wikipedia.org/wiki/Australian_bat_lyssavirus , https://en.wikipedia.org/wiki/Hendra_virus
There is absolutely nothing amazing about covid being able to infect humans, it's exceptional because it can pass from human to human and because it's airborne(ish).
This is a good summary of the current consensus:
It is clear from our analysis that viruses closely related to SARS-CoV-2 have been circulating in horseshoe bats for many decades. The unsampled diversity descended from the SARS-CoV-2/RaTG13 common ancestor forms a clade of bat sarbecoviruses with generalist properties—with respect to their ability to infect a range of mammalian cells—that facilitated its jump to humans and may do so again. Although the human ACE2-compatible RBD was very likely to have been present in a bat sarbecovirus lineage that ultimately led to SARS-CoV-2, this RBD sequence has hitherto been found in only a few pangolin viruses. Furthermore, the other key feature thought to be instrumental in the ability of SARS-CoV-2 to infect humans—a polybasic cleavage site insertion in the S protein—has not yet been seen in another close bat relative of the SARS-CoV-2 virus.
The other big inconsistency is that the epidemic did not become nonticeable in Italy until late February 2020. If COVID was already present in September 2019, why didn't it spread rapidly like it did anywhere else?
[1] https://journals.sagepub.com/doi/full/10.1177/03008916209877...
https://www.who.int/health-topics/coronavirus/origins-of-the...
Origins of the SARS-CoV-2 virus
And unlike the arrticle here, this report is based upon interviews with employees at the lab and various form of documentation provided by the lab. Including health records of the employees.
For more from one of the WHO people:
https://theconversation.com/i-was-the-australian-doctor-on-t...
I was the Australian doctor on the WHO’s COVID-19 mission to China. Here’s what we found about the origins of the coronavirus
In the beginning of January 2020, president Trump was already informed by an advisor who had close contacts in Wuhan that the outbreak was much more severe than China made it look like. But he chose not to act on that, because the USA were in the middle of closing a trade deal with China. However later that month he changed his mind when the first infections in the USA happened, and later even more when a Chinese official came out with a theory that it might actually have been an USA sports team that visited Wuhan in late 2019 that was the source of the Corona outbreak (https://www.nytimes.com/2020/03/13/world/asia/coronavirus-ch...)
So this is not about 'people making this about China', it has been China from the start trying to cover this up and trying to make it about other countries. A more transparent Chinese policy would have given other countries the chance to react early and save thousands of lives.
I looked into these lab origin theories for the furin cleavage site last year. The problem with it being a laboratory insertion was that although performing an insertion is relatively easy once you know what to insert, generally it’s beyond current science to independently create mutations for a specific purpose.
It’s a bit beyond me as a non-biologist but my feeling based on the literature was that the lab origin was unlikely. However it is pushed in certain circles partly for ideological reasons, based on evidence that is plausible at first glance but with a lot more digging not entirely convincing evidence.
However, there didn’t really seem to be much neutral expert analysis of the evidence.
b) Genetic analysis indicates that it most likely came from bats directly to humans, but picked up the ACE2 receptors from a Pangolin virus that was passed back to bats, evolved there and then infected humans. To quote the same nature article I lined above:
However, on closer inspection, the relative divergences in the phylogenetic tree (Fig. 2, bottom) show that SARS-CoV-2 is unlikely to have acquired the variable loop from an ancestor of Pangolin-2019 because these two sequences are approximately 10–15% divergent throughout the entire S protein (excluding the N-terminal domain). It is RaTG13 that is more divergent in the variable-loop region (Extended Data Fig. 1) and thus likely to be the product of recombination, acquiring a divergent variable loop from a hitherto unsampled bat sarbecovirus28. This is notable because the variable-loop region contains the six key contact residues in the RBD that give SARS-CoV-2 its ACE2-binding specificity27,37. These residues are also in the Pangolin Guangdong 2019 sequence. The most parsimonious explanation for these shared ACE2-specific residues is that they were present in the common ancestors of SARS-CoV-2, RaTG13 and Pangolin Guangdong 2019, and were lost through recombination in the lineage leading to RaTG13. This provides compelling support for the SARS-CoV-2 lineage being the consequence of a direct or nearly-direct zoonotic jump from bats, because the key ACE2-binding residues were present in viruses circulating in bats.
and:
Although the human ACE2-compatible RBD was very likely to have been present in a bat sarbecovirus lineage that ultimately led to SARS-CoV-2, this RBD sequence has hitherto been found in only a few pangolin viruses.
Military games / Fort Detrick vaping disease troll was in response to Tom Cotton and co. formally spewing lab leak theory. Note earlier date in Feb.
https://www.washingtonpost.com/politics/2020/02/16/tom-cotto...
US politicized first, when soft measures failed a month after warning Wuhan lockdown. There was ample warning, enough that many of PRC neighbors with high traffic contained well with at least some effort in coordination. PRC position up until then was let science figure it out, Wuhan was very covid19 was first discovered but doesn't mean originated there. The brief domestic deflection in early Feb was possible import from ASEAN. Even early PRC "dis"info campaigns emphasized harsh lockdown not lockdown skepticism. Countries that didn't take Wuhan lockdown seriously got burned. Queue west being prominent source of exporting covid world wide by taking lax measures. This is seen in import statistic of every country that rigorously tracked imported covid cases - PRC exported very little cases, and essentially none few weeks after lockdown. North America / Europe, magnitudes more.
Can't help feeling sad, and bewildered in capacity of humans to cause damage at this level - the havoc this (human-made) virus is inflicting on people - close and faraway.
https://www.cartalk.com/radio/letter/andy-letter
Original section of the episode: https://www.cartalk.com/sites/default/files/bestmoments/2019...
No it isn't.
> The virus entered humans with it's spike protein already fully adapted to the human ACE receptor protein.
1. Is a partially functional (still infectious) spike receptor protein possible? (you don't know, and present no evidence in this rant)
2. How do you know the virus shows "no accelerated evolution"...partially effective viruses would have a lower replication factor, and not become global pandemic, and would not spread far enough to preserved within the human population as anything of interest.
3. How do you know that a natural virus which was only partially effective at replication didn't in fact encounter favorable conditions when it encountered humans, having accidentally been better adapted for them?
> The fact that it doesn't mutate rapidly indicates it is near a strong local optimum.
4. How do you know that the spike protein - which is highly conserved amongst coronaviruses - can even have a range of mutations and still retain function (allowing viral entry to the cell for infectious purposes)? (you don't, research finds that the spike protein has suboptimal binding to ACE receptors - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7239051/)
> This stands in intense contrast to every other zoonotic transfer we know of.
5. Does it? Because no research is proposing this. Research in fact finds that analysis of similar coronaviruses shows that the spike protein is likely the result of multiple recombinations between a few species (https://academic.oup.com/emph/article/2020/1/290/5956769).
> Do we have evidence? What is the probability of this pattern occuring in the case of a natural spillover?
6. Do you? Apparently not because there's not a single shred of peer reviewed research you care to link to support your position here, and you've done none of the legwork to support the logic part of your conclusions.
There has been an extensive analysis by a virologist on Reddit[¹], who claimed that, very simply, SARS-COV2 is a so-called "mosaic" virus, while man-made viruses are inevitably "chimera" ones. The article does not seem to make this distinction.
The virologist also chimed on HN (besides, calling BS on people who were, out of ignorance, spreading false beliefs), but it seems he's not participating to this post.
It'd be best to have the opinion of a specialized scientist, in order to to have scientific clarity before starting the political arguments.
[¹]=https://www.reddit.com/r/science/comments/gk6y95/covid19_did...
What makes you think that they are a concept developed by the CIA?
> Such furin-mediated activation is unusual in that it occurs in part during virus entry. Our findings may explain the polytropic nature, pathogenicity, and life cycle of this zoonotic coronavirus.
MERS-CoV uses furin cleavage of S1/S2 but it does not bind to ACE2 like SARS-CoV-2.
The link you provided does discuss the probability of the virus accidentally leaking from a laboratory, however the reasons provided does not really provide much facts, seemingly more speculation (except for facts regarding who we think is patient zero):
"The WIV, and Dr. Zhengli-Li Shi’s lab group, are extremely well-respected in the virology community. As well respected as many US scientists.
● All the WIV’s sampling of bats and the genomes that they find in bats are publicly available information. Why isn’t SARS-CoV-2 on any of those lists? We would know.
● This doesn’t look anything like any laboratory accident that we’ve seen before.
● The evidence we have points to Patient Zero being nowhere near the City of Wuhan." (https://drive.google.com/file/d/1kAHSEx9-eIyVIahczH8itHaUm9j...)
Also: major changes in he spike protein could impact the ability of the virus to infect humans, so -- there is that.
https://2017-2021.state.gov/fact-sheet-activity-at-the-wuhan...
However, the evidence is pretty clear that this was found and published earlier. It was originally described as "BtCoV/4991" and it was described and published as far as I can find as far back as 2016. (The name was changed to RaTG13 to describe that it was collected in 2013 in Tongguan).
https://www.ncbi.nlm.nih.gov/nuccore/983856042 <-- partial RaTG13 sequence in 2016
"The natural emergence theory battles a bristling array of implausibilities."
This is a fantastic article, but amazingly almost all of it is year-old news. Most of this was known in March 2020, and nearly all of it by the end of 2020. How does it take so long for the truth to win?
I published a meta-analysis covering much of the same ground in November 2020 and this was only after waiting and expecting for several months that someone with a better platform would do so first. The article above covers the most important points but the story does go deeper: https://followtheplot.org/covid19
I've done some separate reading that this is a legitimate way that viruses can adapt to a new species, but I don't have any background to evaluate the argument much beyond face value.
Some of the adjacent comments shed some doubt there as it sounds like bats aren't a plausible source because of the spike protein genetics.
https://www.independentsciencenews.org/commentaries/a-propos...
In the beginning, they arresting doctors in Wuhan who spoke about it https://en.wikipedia.org/wiki/Li_Wenliang
[1] https://twitter.com/PeterDaszak/status/1197631383470034951?s...
It was used as an example of “fake news”: https://www.nytimes.com/2021/02/02/technology/biden-reality-...
> “ Hoaxes, lies and collective delusions aren’t new, but the extent to which millions of Americans have embraced them may be. Thirty percent of Republicans have a favorable view of QAnon, according to a recent YouGov poll. According to other polls, more than 70 percent of Republicans believe Mr. Trump legitimately won the election, and 40 percent of Americans — including plenty of Democrats — believe the baseless theory that Covid-19 was manufactured in a Chinese lab.”
What makes my blood boil about this is the NYT is supposed to be able to tell the difference - this kind of self righteous stupidity explains the rise of trump and distrust of media orgs more than anything else, it’s what lays the groundwork for baseless conspiracy.
Yes there were dumb conspiracies about a manufactured and intentionally released bio weapon, but the accidental release from the lab that actually exists and studies these exact viruses in Wuhan and the additional context of the lies from the CCP about the Pangolin (and just general suspicious blocking of access) made it a reasonable hypothesis.
What irony that in a piece pushing support for a “reality czar” (presumably to censor certain stories?) is the position of the NYT so divorced from reality itself.
Pair this with the WHO rep being afraid to say the word Taiwan and it looks bad there too: https://www.reuters.com/article/us-health-coronavirus-who-ta...
In a lot of ways it feels like the west is under constant attack from disinformation and self-inflicted censorship (movies, Apple, nba, etc. all afraid to be critical of the CCP) and doesn’t even realize what’s going on. I think the CCP understands what they’re doing.
This is an ideological war, we’re already under attack, and the west is losing. The CCP (and Russia to a lesser extent) understand where our vulnerabilities lie and they’re exploiting them.
Edit: Whenever this comment reaches +1 it’s quickly downvoted to -2, dang - if you see this do you have a way to tell if this is legitimate (users behaving as they wish to) or something else? I only consistently see this behavior on comments that mention the CCP.
2020 will be forever the year I lost total trust in mainstream media. It's one thing to just "get it wrong" it's an entirely different thing when the powers that be are actively trying to promote a false narrative.
And then to turn around and label actual journalism and truth seeking as "conspiracy-theorist" and "crack pots" it is just too much to bear.
Filling the news with endless critiques and shaming of the proper way and material of mask to wear but deflect any attempts at uncovering, How the Hell this thing Started in the First Place!
They have become the anti-thesis of news and journalism and a driving force of division in the United States.
A pillar of democracy and free speech has become the thing it was intended to prevent and is now firmly a Fifth Column [1].
So, basically, you're saying that (many, we know how contagious covid 19 is) people got sick and put into hospital/died with a novel respiratory disease in another (or several other) chinese cities first. However, that was covered up or unnoticed _until_ it reached wuhan, and for some reason a researcher who works with coronaviruses at the lab saw a sick patient (at the hospital?), realized "that looks like a novel coronavirus" and decided to raise the alarm? Additionally, after that only Wuhan got shut down, while the other city or cities which should have had a raging epidemic by now still went unnoticed?
That's what I mean, these other theories to explain away what is the most staightforward explanation makes no sense, and invokes too many unlikely scenarios or coincidences.
Regarding gain-of-function, see [nature article from 2015](https://www.nature.com/news/engineered-bat-virus-stirs-debat...) questioning the safety of gain-of-function research, and the article that [triggered the reaction](https://www.nature.com/articles/nm.3985). Part of that research took place in the Wuhan lab.
(Then there are the conflicts of interest of the WHO investigator Peter Daszak, who is very quick to discredit any theory that the virus might have escaped from the lab...)
Again, this is a farce, and it would almost be funny if it weren't for all the dead and the generally shitty situation for most of the world at the moment.
I just have a hard time understanding why so clear evidence of the epidemic starting outside Wuhan is missing from the debate, so I'd appreciate if you could comment on it.
“Shi was surprised that the outbreak was local, she said: “I had never expected this kind of thing to happen in Wuhan, in central China.” The bat hiding places that she’d been visiting were, after all, as far away as Orlando, Florida, is from New York City. Could this new virus, she wondered, have come from her own laboratory? She checked her records and found no exact matches. “That really took a load off my mind,” she said. “I had not slept a wink for days.””
https://www.scientificamerican.com/article/how-chinas-bat-wo...
Unfortunately you won't find it on Google Maps but anyone who is able to read Chinese can check this themselves. All the early cases were centered around this area, including the hospital that treated the first cases. It's absurd that this is almost never talked about anywhere. On the CDC website they had an open position looking for a researcher to study, among others, exactly the kind of bat CoV that's been identified as most closely related to SARS-CoV-2. This has since been deleted but it could still be accessed during the early days of the outbreak.
> https://www.sciencedirect.com/science/article/pii/S187350612...
They exist in the human HCoV-HKU1, HCoV-OC43, MERS-CoV and appear to have evolved independently at least 6 times in betacoronaviruses.
Furthermore while this article claims that the furin cleavage site has not found in any sarbecoviruses, that is now outdated information:
> "Evidence for SARS-CoV-2 related coronaviruses circulating in bats and pangolins in Southeast Asia"
> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7873279/
Both RacCS203 (91.5% similar to SARS-CoV-2) and RmYN02 (93.3% similar to SARS-CoV-2) have furin cleavage sites. So we're up to 7-to-9 times now that evolution has evolved a furin cleavage site in betacoronaviruses, including 3 sarbecoviruses that may or may not be directly related.
The whole "furin cleavage site is an indication of human engineering" argument is just falsified at this point.
> To investigate the importance of the spike polybasic CS of SARS-CoV-2 (PRRAR), a number of spike mutants predicted to modulate the efficiency of furin cleavage were generated (Fig. 1a), including: substituting two upstream arginines to produce a monobasic CS similar to SARS-CoV spike (monoCS), replacing the tribasic CS with the furin CS of a highly pathogenic H5N1 avian influenza haemagglutinin containing seven basic amino acids (H5CS) and two naturally occurring deletions seen following passage in Vero E6 cells and/or in clinical isolates21,26. The first deletion removes eight amino acids including all three arginines of the PRRAR site (ΔCS), while the other removes five flanking amino acids but retains the tribasic CS (Δflank). The mutations were engineered into a spike expression plasmid to enable cell surface expression and generation of coronavirus lentiviral PVs. In addition, to study the importance of the PRRAR motif in the context of live virus, we used a naturally occurring Vero-cell-adapted mutant SARS-CoV-2, ΔCS26. This variant and the wild-type (WT) virus from which it was derived were cloned by limiting dilution to enable studies using individual genotypes.
This is the horror of in vitro and in vivo viral lab research and the result is a magnificent advancement of our understanding of SARS-CoV-2, the furin cleavage site, and its role in TMPRSS2 assisted membrane entry. This research follows the equally eye-opening paper covered in TWiV 715 that explained why hydroxychloroquine (HCQ) failed; Vero E6 cells lack TMPRRS2 so HCQ fully blocks entry via endocytosis. It should be noted that this study includes MERS-CoV which also has a furin cleavage site; falsifying one of the claims of Wade's article.
Regardless, lab experiments begin with one or more viral isolates and molecular clock techniques should show that the original Wuhan variant has almost identical non-coding genome segments compared to existing lab isolates. The RaTG13 sequence is a very distant relative using this measure. Also, RaTG13 is not an isolate, only an RNA sample collected in wild bat anal swabs. Conflating viral isolates with RNA samples seems to be a common error; an entry in a genetic database does not imply that a viable viral line exists in a lab. A RaTG13 lab isolate would have been an important achievement to further our scientific understanding.
I'm confused by the dismissals of the natural origins hypothesis. The horseshoe bat roosts, that are studied, are mostly found in or near Kunming, Yunnan. This lush wild area is part of the Lancang/Mekong River watershed/ecosystem shared by nocturnal bats and nocturnal arboreal mammals like palm civets, pangolins, and raccoon dogs. The nearby villages contain people engaged in guano collection, the wildlife trade, and domestic livestock farming.
The average incubation time of COVID-19 is 4.5 days. Armed with Google maps and a basic understanding of planes, trains, and automobiles we can gauge travel time from Kunming Airport to either Wuhan Tianhe International Airport (2 hr 5 min) or Guangzhou Baiyun International Airport (2 hrs). In 2003, SARS-1 emerged in Guangzhou (near Hong Kong) and the now demonized Dr. Zheng-li Shi and her team traced the origins to palm civets (the intermediate host). Why is this so hard? Why do we not ridicule the assumption that travel between major Chinese transportation hubs must leave a wake of infections along the path?
Finally, Wade's article mentions a U.S. State Department claim [2]:
> The U.S. government has reason to believe that several researchers inside the WIV became sick in autumn 2019, before the first identified case of the outbreak, with symptoms consistent with both COVID-19 and common seasonal illnesses.
If true, this is an important early super-spreader event but the remainder of the release consists of a facile analysis performed by people more knowledgeable in geopolitics than science.
[1] https://www.nature.com/articles/s41564-021-00908-w
[2] https://2017-2021.state.gov/fact-sheet-activity-at-the-wuhan...
The point is that we should consider both the cost and the benefit of any regulation, in an expected value sense. Cars do kill people, but they also provide transportation that we've judged is worth that cost. But there's little indication that the WIV's (USA-funded!) risky research has delivered any significant benefit--the predicted coronavirus pandemic has indeed occurred, whatever the cause, and has anything from the WIV's work help us deal with that? On the other hand, even a small chance that their work caused this pandemic is a hugely negative expected value.
Long before the pandemic, there was obscure, academic debate over whether certain types of research with potential pandemic pathogens were worth the risk. Even with the evidence available at that time, I believe the 2014 ban was good, and its 2017 lifting was bad; but that debate now that takes on terrible new significance.
And how does that explain its affinity for human ACE2? At least initially (right after it makes the zoonotic jump), the virus would probably show highest affinity for its animal host, and lower affinity for human ACE2. But SARS-CoV-2 shows highest affinity for human ACE2, and only primates with ACE2 very similar to humans show comparable affinity:
> The very high classification had at least 23/25 ACE2 residues identical to human ACE2 and other constraints at SARS-CoV-2 S-binding hot spots (Materials and Methods). The 18 species predicted as very high were all Old-World primates and great apes with ACE2 proteins identical to human ACE2 across all 25 binding residues.
I also downvoted the comment, by the way, so I can explain at least one of the downvotes. It wasn't because I disagree with you. It was because ideological battle is against the HN guidelines: https://news.ycombinator.com/newsguidelines.html.
When your blood is boiling, that's not a good state in which to post to HN. Better to wait for it to cool and then post in the key of curiosity. That's what HN is supposed to be for. I mean, I know you know this. But it's not so easy in practice, especially when you feel like you're under attack and your side is losing [1].
It's in your interest, though. Boiling-blood comments are like a Maxwell's demon who not only has energy to separate molecules into disjoint compartments, but enough left over to keep them buzzing angrily. You'll get upvotes and praise from people who already agree with you, and downvotes and anger from people who already disagree. But what you should be doing instead, if you want to help your own view, is trying to persuade the persuadable. That requires an entirely different, molecule-enticing strategy. A Maxwell's angel perhaps?
---
[1] I don't know how many of us would have guessed it, but one thing has become apparent from trying to keep HN interesting: functioning curiously requires developing one's ability to experience difficult feelings and somehow carry them and not let them drive you into reaction—which is a pretty deep human task. It turns out that simply trying to optimize HN for one thing—curiosity—has counterintuitive consequences, some of which ask a lot of us.
https://hn.algolia.com/?dateRange=all&page=0&prefix=false&qu...
I wrote about some of those consequences here, if anyone is interested in reading further: https://news.ycombinator.com/item?id=23308098.
I'd like to be able to share an article from a website that doesn't also write about Trump and facebook.
This is incorrect.
Bat (Rhinolophus) sarbecoviruses have been isolated and sequenced in Hubei:
https://www.ncbi.nlm.nih.gov/nuccore/DQ648856
https://www.ncbi.nlm.nih.gov/nuccore/DQ648857
The closest KNOWN bat sarbecovirus was found in Yunnan, but it was only 96% identical. That doesn't preclude the actual 98-99% identical progenitor virus of SARS-CoV-2 from living in Hubei.
Rhinolophus bats are all over southern China, and neighboring countries with a very wide range, and the all carry SARS-CoV-like viruses.
Also nothing precludes the species jump from bats to farmed animals happening in Yunnan and then infected animals being transported to farms in Hubei.
I also never mentioned pangolins or wet markets because we know at this point that neither of those are related. The animals to focus on would be minks and other mustelids or raccoon dogs or other farmed animals.
And we already know that SARS-CoV-1 likely originated in bats in Yunnan (where the "WIV1" coronavirus was found) while the leap to humans from an intermediate animal is thought to have happened in Guangdong. Again we have here a problem of "how did the virus in Yunnan jump to people 700+ miles away?" but in the SARS-CoV-1 case there's no weapons laboratory distraction. It happened back then with SARS-CoV-1 so therefore any objections you can have about coronavirus jumping species and geography is just falsified. It is unlikely clearly or this would just happen every other year.
https://www.pnas.org/content/117/36/22311
Evolution doesn't require anything beyond "good enough", but it's surprising for a virus to be better-adapted to humans than to its animal hosts at the moment of its zoonotic jump--before the jump, where could that pressure come from? I don't think this is determinative, but it points weakly in favor of lab origin (e.g., from culture in human cells or in mice genetically engineered to express human ACE2).
https://www.breakingasia.com/wp-content/uploads/Wuhan-Virolo...
A virology lab studying the human transmissibility of bat corona viruses ~10km away from the purported epicenter of the outbreak of a bat related coronavirus is notable.
He retweeted a tweet that pointed out Nicholas Wade has been accused in the past of grossly misrepresenting research.
https://www.sciencemag.org/news/2014/08/geneticists-decry-bo...
REad more: https://www.genxsentinel.news/govt-of-india-has-so-far-provi...
Out of all the wet markets that serve that much population, the coronavirus just happened to appear at the market nearest to the lab studying coronaviruses. To have such a coincidence is like winning the lottery.
It's not evidence, sure, it's correlation at best. But this alone should make you investigate that lab much much better, it should be the first possible cause you research.
But looking at the lab first might be hard if you have a severe conflict of interest https://www.taiwannews.com.tw/en/news/4119101
I am not saying this to "make China pay". After all, the US itself was sponsoring coronavirus research at that lab. But we should establish a worldwide safety standard in dealing with such research, and establish periodical inspections. Just like we do with Nuclear power plants, only better.
> We have done bat virus surveillance in Hubei Province for many years, but have not found that bats in Wuhan or even the wider Hubei Province carry any coronaviruses that are closely related to SARS-CoV-2. I don't think the spillover from bats to humans occurred in Wuhan or in Hubei Province.
https://www.sciencemag.org/sites/default/files/Shi%20Zhengli...
Anyways, the point isn't that a natural zoonotic jump in Wuhan is perfectly impossible. Even if we assumed (wrongly, at least if you believe Dr. Shi) that natural zoonosis was equally probable in any city in China, the emergence of SARS-CoV-2 in Wuhan is still evidence in favor of a lab accident. To a good first approximation, the WIV does 100% of the research on novel SARS-like viruses in China, so an outbreak due to a lab accident would probably emerge there. So whatever your Bayesian prior was for natural vs. lab accident, its emergence in Wuhan should update that by a factor of ~100 (i.e., the population of China divided by the population of Wuhan).
And I'm not sure why you think farmed animals are likely intermediate hosts? China has been sampling extensively, and while it's not necessarily easy to find the intermediate host (e.g., for Ebola), that should be far easier in a factory farm than in the wilderness. So why haven't they found that?
Finally, I don't think anyone brought up weapons here except you? That seems like a deliberate conflation, introducing outlandish theories for which no evidence exists ("SARS-CoV-2 was designed as a bioweapon") to discredit the more likely theory actually being discussed ("SARS-CoV-2 originated from a lab accident during internationally-funded basic research").
For example, here's another one of those odd coincidences that gets easily dismissed as a conspiracy theory: September 2019 there was a pandemic wargame called "Outbreak 2019", specifically based around an infectious disease that causes respiratory failure.
https://www.military.com/daily-news/2020/04/01/naval-war-col...
Mink seem very unlikely to me, since I've seen papers reporting evidence of host adaptation on mink farms:
https://academic.oup.com/ve/article/7/1/veaa094/6025194
So if the virus first evolved in mink, it would have to have evolved enough in humans not just to favor human ACE2 but also to lose its affinity for mink (to the point it has to regain it later), all during that couple months of cryptic spread.
And do you really think China is doing a bad job looking for the intermediate host? I don't think that's impossible--for example, the true origin could be some agricultural practice so horrible that they consider the present uncertainty better than disclosing that. Lab origin has become strongly associated with anti-China political sentiment, though. (That seems stupid to me, considering that the USA was funding the WIV; but here we are.) So I'd be surprised that the CCP would pass up a chance to disprove that.
In fact, the paper [3] cited in the top comment has the following response to the Wu and Zhao paper you cited:
> The recent acquisition of the FCS by SARS-CoV-2 via a natural insert was proposed by Wu and Zhao (2021) on the basis of the existence of FCS in other, more distant Betacoronaviruses with different loop positions to SARS-CoV-2 and the existence of a partial natural insert in the same region in RmYN02 (Zhou et al. 2020a). The reliability of the conclusions of Zhou et al. (2020a) has been questioned by Deigin and Segreto (2020), who particularly challenge the claim that RmYN02 has an insertion around the site of the FCS insertion in SARS-CoV-2 and instead point to a two amino acid deletion in RmYN02 at that locus. Therefore, RmYN02 should not be used as evidence of the natural origin of SARS-CoV-2′s FCS until its claimed insertion is properly validated.
Disclaimer: I’m no biologist/virologist.
[0] https://www.sciencedirect.com/science/article/pii/S187350612...
[1] https://doi.org/10.1016/j.cub.2020.05.023
[2] https://arxiv.org/abs/2012.00627
[3] https://link.springer.com/article/10.1007/s10311-021-01211-0
