> Historically, there have been far, far more documented lab leaks of SARS-CoV than there have been animal-human jumps
No. First of all, there were many jumps of SARS from animals into humans, over a period of months in which the markets containing infected animals were open. Second, while there were a few leaks of SARS-CoV after it had been discovered and was being grown in large quantities (these leaks were recognized immediately, too), there is no precedent for a previously unknown coronavirus leaking.
> It is very possible that the virus was both zoonotic in origin, and leaked from the lab.
Not really. If the virus is natural in origin (which is a certainty now) and completely unknown before the initial outbreak (also a virtual certainty now), the chance that it somehow entered a lab, unknown, and then exited again are basically zero, compared to the chance that it spilled over in any one of the many millions of daily interactions between humans and wild or farmed animals.
They were selling farmed wild animals that we know can carry SARS-CoV-2 at the Huanan market, and that's where the initial outbreak was centered. In contrast, there's zero evidence for a lab leak, and not for lack of searching. There's simply no evidence that anyone at the Wuhan Institute of Virology had or knew about this virus before the outbreak, and we have a very good idea of what the WIV was researching.
> First of all, there were many jumps of SARS from animals into humans, over a period of months in which the markets containing infected animals were open.
Can you point me to one or two cases you are talking about, please?
They may be referring to the study below [0]. This showed that several genetic variants (lineages) of SARS-CoV2 were identified in infected people associated with the market, indicating 1) that the virus was already circulating among people before the epidemic took off, and 2) that there was more than one transmission event.
Note that no comparable data associates SARS-CoV2 with the lab in Wuhan.
>we inferred separate introductions of SARS-CoV-2 lineages A and B into humans from likely infected animals at the Huanan market (38). We estimated the first COVID-19 case to have occurred in November 2019, with few human cases and hospitalizations occurring through mid-December. [...] the evidence presented here that lineage A, like lineage B, may have originated at the Huanan market and then spread from this epicenter into the neighborhoods surrounding the market and beyond.
>We show that SARS-CoV-2 genomic diversity before February 2020 likely comprised only two distinct viral lineages, denoted “A” and “B.” Phylodynamic rooting methods, coupled with epidemic simulations, reveal that these lineages were the result of at least two separate cross-species transmission events into humans. The first zoonotic transmission likely involved lineage B viruses around 18 November 2019 (23 October to 8 December), and the separate introduction of lineage A likely occurred within weeks of this event.
For the rec, comment I'm replying to highlights two simultaneously released papers that both include 4 of the 5 authors of the 2020 paper, Proximal Origins, that is in question by the Nate Silver piece that headlines this HN post. (The 5th author, Lipkin's "view has changed":
"The revelation that the WIV was working with SARS-like viruses in subpar safety conditions has led some people to reassess the chance that SARS-CoV-2 could have emerged from some type of laboratory incident. “That’s screwed up,” the Columbia University virologist Ian Lipkin, who coauthored the seminal paper arguing that covid must have had a natural origin, told the journalist Donald McNeil Jr. “It shouldn’t have happened. People should not be looking at bat viruses in BSL-2 labs. My view has changed.”
SARS repeatedly spilled over into humans during 2002-2003, until the markets were shut down and the infected animal populations were culled. A review on SARS [0] describes how many independent clusters of SARS popped up over a period of months, spread across different markets in the Pearl River Delta:
> Between November 2002 and February 2003, the first cases or clusters of SARS appeared in several independent geographic locations in the Pearl River Delta region in southern Guangdong, and suggested multiple introductions of a virus or similar viruses from a common source. Several of the early cases were reportedly associated with occupations that involved contact with wildlife, including handling, killing and selling wild animals as well as preparing and serving wildlife animal meat in restaurants (Xu et al. 2004). Moreover, a study of early SARS cases (i.e. those with disease onset prior to January 2003) compared to those identified later in the outbreak found that 39% of early-onset cases were food handlers, whereas only 2%–10% of cases between February and April 2003 were associated with this occupation.
The review goes on:
> It was observed that early cases of SARS occurred independently in at least five different well-separated municipalities in Guangdong Province. The study also found that early patients were more likely than later patients to report living near a produce market, but not near a farm, and nine of 23 (or 39%) early patients were food handlers with probable animal contact.
The review also discusses how many SARS spillover events were not recognized at the time:
> Several studies revealed a higher than normal seroprevalence of SARS-CoV antibodies among wild animal traders. Guan et al. (2003) found that eight of 20 (40%) wild animal traders sampled from a market in Shenzhen, Guandong, in 2004 had anti-SARS-CoV antibodies in comparison to 1 from 20 (5%) vegetable traders from the same market. Yu et al. (2003) analysed serum samples taken on May 4, 2003 from animal traders in three different live animal markets in Guangzhou. Out of 508 animal traders surveyed, 13% had antibodies to SARSCoV; 72% of traders of masked palm civets ( Paguma larvata ) were seropositive. Interestingly, none of the animal traders had SARS or atypical pneumonia diagnosed during the SARS outbreak in Guangdong, suggesting asymptomatic infection by SARS-CoV or a closely related SARS-like coronavirus.
SARS probably spilled over countless times into humans during 2002-2003, because there was a large population of farmed animals that had it, and very little was done to cut off the spillover source for months.
This is a key difference from SARS-CoV-2. This outbreak was detected much more quickly (because of China's experience with SARS), and the very first thing the authorities did was to close the Huanan market and crack down on farms that raise the types of animals that are most likely to be involved in the spillover.
There were countless spillover events for the original SARS. To this day, it's not known precisely how many SARS spillover events there were, because they were so numerous and tracing was so poor back then. In a different comment in this thread, I cited a review article that goes over the evidence for widespread spillover events of SARS in 2002-2003.[0]
The gist of it is that SARS popped up independently at numerous markets, dotted across the Pearl River Delta. SARS infection was very common among palm civet traders in the region (it's even possible that most of them became infected).
The lab leaks came later, after huge interest emerged in the new virus and it started to be cultured in large quantities in many labs. Those leaks were extremely rare compared to the spillover events, they were immediately detected, and they led to much stricter lab security practices. But the relative probability of a novel virus that nobody even knows they have initially leaking from a lab vs. spilling over from large animal populations that host the virus is basically nil.
You're mixing up animal > human transmission, and zoonotic events. They are not equivalent. Human SARS spike protein RBD could bind palm civet ACE2, but not vice versa. Palm civets (and other animals) could act as reservoirs for human SARS, (as well as non-human SARS, which contributed to the zoonotic event), but that's not the same as a new virus jumping species. It's more like getting rabies from a raccoon.
It's possible that the original SARS jumped 3 times total, based on the genetic evidence, but the later two we don't really know because of the hinam -> animal route. Still, with the number of laboratory acquired infections of SARS-CoV-2, it doesn't really tip the scales.
If rabies were a novel virus that had never infected humans before, you could make the comparison. SARS was a novel virus, which spilled over into humans in a very similar manner to SARS-CoV-2 (wild animal markets in a major Chinese city).
> It's possible that the original SARS jumped 3 times total, based on the genetic evidence
As the review I cited explains, the epidemiological and serological evidence makes clear that SARS independently jumped over to humans at many different locations, over the course of months.
> It's possible that the original SARS jumped 3 times total, based on the genetic evidence
You're saying animal -> human transmission of a human virus is equivalent to animal -> human transmission of a new virus. Those are two *extremely* different things. The palm civet SARS spike protein RBD did not gain the ability to bind human ACE2 many times. In fact, the evidence for that seems to only be a single time. The remaining two suggested origin events show mutation of the existing virus, followed be retransmission across species barriers.
Those are two completely different types of events.
> You're saying animal -> human transmission of a human virus is equivalent to animal -> human transmission of a new virus.
You're making up an entirely arbitrary distinction.
> The palm civet SARS spike protein RBD did not gain the ability to bind human ACE2 many times.
You have no idea if this is the case. Most of these small outbreaks were not analyzed in detail (or even known about until well after the fact). The evidence shows that the virus was able to jump from animals to humans numerous times, and possibly spread in small clusters.
No, they're two very different things, because one involves an adaptation. Once adapted, the rules of the game for cross-species transmission events are completely different.
Or do you maintain that a combination cross-species transmission and adaptation to the new host is as common as cross-species transmission of already-adapted viruses?
I see that you're trying to imply that SARS-CoV-2 was pre-adapted to humans, while SARS wasn't, so this is going in a conspiracy-theory direction.
I guess the Wuhan Institute of Virology also produced a special deer-adapted version which they released into the wilds of North America, and a mink-adapted version they released on farms in Denmark, and a hamster-adapted version, and a cat-adapted version, and on and on. Both SARS and SARS-CoV-2 have shown an ability to infect a range of different species.
You haven't made a coherent point yet. You're trying to draw a distinction between zoonosis and animal-to-human transmission. The former literally means the latter.
And then claiming that the numerous independent clusters of SARS that popped up in wild animal markets across the Pearl River Delta aren't examples of zoonosis?
There are numerous cornaviruses that infect humans as well as bats and birds, and have done so for thousands of years at least. Animal-to-human transfer of novel viruses is by far the most common cause of novel epidemics.
>Many human coronaviruses have their origin in bats.[75] The human coronavirus NL63 shared a common ancestor with a bat coronavirus (ARCoV.2) between 1190 and 1449 CE.[76] The human coronavirus 229E shared a common ancestor with a bat coronavirus (GhanaGrp1 Bt CoV) between 1686 and 1800 CE.
My point is that we don't have any documented anything for the first couple hundred thousand of years of humanity's existence, and we encountered the most horrific viral and bacterial infections, many of which caused unthinkable mass deaths. They were so awful we attributed them to God(s) as punishment for our bad behavior. None of them have documented microbiological origins. Some would have some from spontaneous mutation in humans and many would have come from animals. They are de facto not lab leaks, so the fact that we have some lab leaks documented in the last few decades isn't really convincing. There is nothing there that makes a zoonotic origin less likely.
Here's a scientist who said we couldn't dismiss the lab leak, and asked for more research, which he did.
The early cases are clustered around the market. I know the market and the lab are "close" on a global scale, but the details matter. They are 30km apart, about a 45 minute drive in traffic. Looks about as clear as John Snow's map of cholera outbreaks in London.
That article is from 2021, but he stands by it in 2023:
"What is the chance that a big Chinese city like Wuhan would have a lab doing the kind of research that has come under suspicion? The answer is, the vast majority of the biggest cities in China have labs involved in such research. If COVID had emerged in, say, Beijing, there would be no fewer than four such labs facing suspicion."
Edit:
2 things.
It's important to rule out that the idea that this could only be engineered, which would imply a definite lab origin. That is why engineered viruses come up. A non-lab leak is certainly plausible, and a lab leak is not ruled out.
There are labs all over China, there are markets all over China. The overlap of cities having both is significant. Viruses appear in larger, denser population centers. The "next thing" was very likely to appear in a city with a lab. The thing is, it's not very close to the lab. There's a large cluster around the market.
Lab theory doesn't have much going for it. It's not actually that close to the epicenter. There are labs everywhere. SARS is widely studies.
Sure some viruses have long incubation periods, but that would show as far less of a tight cluster around the market. Your hypothesis seems to be that it spread from lab distantly because of incubation time, then stopped spreading distantly once it reached the market? That does not make sense.
>Your hypothesis seems to be that it spread from lab distantly because of incubation time, then stopped spreading distantly once it reached the market? That does not make sense.
It's not my hypothesis, I'm just pointing out the evidence is circumstantial and the language used by virologists is precisely engineered to lump together strong evidence that proves one thing (that the virus was zoonotic in origin) with weak evidence they want to claim proves another thing (that it couldn't have been a lab leak). It's dishonest language and it drives me nuts, because people aren't sheep or idiots, can find the inconsistencies, and will further have their trust in institutions eroded.
This whole debacle reeks even more when you look at the timeline. These claims were coming out before even that circumstantial evidence was available, when this really truly was just a best guess because it's how we think the last SARS operated.
My personal opinion is that:
1) We'll never have any better evidence than what we have now (so we'll never have any good evidence, short of the Chinese govt being hacked)
2) It doesn't really matter because both are plausible and so our safety models should include both
3) The thing of real importance here isn't what is being debated, but rather how the debate itself was performed, and what it says about authority, institutions, honesty, and elitism in the scientific community.
> 3) The thing of real importance here isn't what is being debated, but rather how the debate itself was performed, and what it says about authority, institutions, honesty, and elitism in the scientific community.
This! This is the point of Silver's piece. Whether or not the virus escaped a Wuhan lab, the summary dismissal of the hypothesis as an conspiracy of cranks, without engaging on the facts, _reinforces the legitimacy of crank-fueled conspiracies_.
I'm being very precise to avoid conflating lab leak and natural origin. There is a possibility those are the same thing. The virus could have been discovered in nature, brought to a lab, and leaked. I personally find this whole debate pretty boring, but it really worries me how frequently people mix this up. These two things are not exclusive. Argument in favor of one does not invalidate the other.
Re: a few specific points.
>The early cases are clustered around the market. I know the market and the lab are "close" on a global scale, but the details matter. They are 30km apart, about a 45 minute drive in traffic. Looks about as clear as John Snow's map of cholera outbreaks in London.
This is a bit of a trap. From that article:
>What about cases near the Wuhan Institute of Virology (WIV), which is more than 10 miles from the market? "There are no cases around the WIV," Worobey says. "If the outbreak did start in the lab, the bottom line is, it would be odd for it not to be spreading from there rather than from elsewhere."
The thing here to consider is that, lets say someone gets an accidental exposure. There's an incubation period, in which you are not shedding. Then you move around. Epidemiological data only shows where the first human-to-human transmission happened, not where the animal-human jump happened. Since you aren't immediately infectious after contracting the virus.
Re:
>"What is the chance that a big Chinese city like Wuhan would have a lab doing the kind of research that has come under suspicion? The answer is, the vast majority of the biggest cities in China have labs involved in such research. If COVID had emerged in, say, Beijing, there would be no fewer than four such labs facing suspicion."
SARS-CoV (the original) notoriously escaped a Beijing lab, not once, but twice.
SARS-CoV also has the added advantage of being much easier to track, because the symptoms are so severe. With SARS-CoV-2, the symptoms are so mild, it's unlikely most people would think it was anything but a cold. Whether someone that worked at a virology institute would think that is a matter of some debate, but people have died from laboratory exposures before because they thought they had a benign illness, so it certainly has happened.
The problem is, people aren't having a genuine discussion. The communication goes something like this: someone says something about lab leak, and gets shut down by saying "the science says animal origin was more likely". The scientists are saying "the data says this was likely an animal to human transmission". But if you dig in on either of those points, things get shakier and shakier. The data that the virus evolved in animals, strong. The data that the virus evolved in any one specific species - less strong. The data that the virus evolved in an animal species that was in the wet market, even weaker. The data that the virus evolved in an animal species at the wet market, and then jumped from animals to humans at the wet market? Basically non-existent - circumstantial at best.
The only piece of data in that tree that would directly contradict the lab leak hypothesis is that last little bit of data. But it all gets wrapped up and packaged into the wordplay of "the data says the virus jumped to humans from animals", probably unintentionally by some, intentionally by others. The wet market hypothesis began because SARS had been found to transfer at a wet market in the past. But, that data has never been super convincing to begin with (this type of data never is, it was a full year after SARS-CoV 1 that antibodies were detected in civets), and there was no direct evidence of the wet market with SARS-CoV-2, so the hypothesis started out as pattern matching with an n=1 (SARS-CoV the original). Whereas, pattern matching with n=4 (or more) for lab leak works just as well.
Also frustrating is that not being able prove one hypothesis doesn't de facto validate the other. The hypotheses aren't even totally orthogonal! Only in very specific cases are they orthogonal, and those cases contain the weakest evidence of all the evidence in all categories.
The featured article is talking more about the conversation, and the nuances of the conversation, than it is the absolute truth of the matter. There will never be an answer, other than that "both are possible".
Re: the "spirit" of your point, if you will, which I interpret at something like "there are many more species than just humans, therefore most viruses evolve in other species and jump to humans", I certainly agree, but then we went and tipped the scales pretty badly by rounding up these viruses and putting them in close proximity to humans. And while we've been recording data, there have been far more lab leaks than there have been zoonotic events. So that argues that in the 20th and 21st centuries, we have, artificially, changed that calculation.
Historically, there have been far, far more documented lab leaks of SARS-CoV than there have been animal-human jumps.
People that wish to shutdown lab leak conversation are quick to mix in engineering. Lots of less educated people can't tell the difference.
It is very possible that the virus was both zoonotic in origin, and leaked from the lab.