Viral: A Review
A reconsideration of the evidence for the laboratory origins of SARS-CoV-2.
Alina Chan and Matt Ridley, Viral: The Search for the Origin of Covid-19 (Harper: New York, 2021). 416 pp. ISBN: 978-0063139121. $19.99.
Something happened in 2019, probably towards the middle of the year. It might’ve been a single event, or perhaps a series of them. If it was an accident, it’s very possible that the people most directly implicated weren’t aware at first; some of them might still be uncertain about their responsibility. If it was deliberate, it’s unlikely anybody intended – let alone envisioned – what actually came to pass. Most people with subject expertise know or suspect that scientists are directly implicated in this event, but few will discuss it openly. I am talking, of course, about the release of SARS-CoV-2 into the human population and the origins of the Corona pandemic.
Alina Chan and Matt Ridley’s Viral is, as far as I know, the only book from a major trade publisher to consider the problem of virus origins in anything approaching an objective light. Its treatment is necessarily compromised. Viral appeared in November 2021, as the mass vaccination campaign lent new political utility to virus terror and encouraged a sudden openness to lab-leak theories. Throughout Viral, from their dedication to “the people who have suffered and lost during the Covid-19 pandemic” to the final pages, Chan and Ridley take every opportunity to talk up the grave risk of Corona infection. More seriously, they undermine their own analysis by striving everywhere for an exaggerated moderation, often failing to draw the conclusions demanded by their own evidence and burying the lede. Probably Harper editors are as much to blame for this as the authors; the effect is to create a false equivalency between the natural and artificial origins theories, and to present an unnecessarily attenuated case for laboratory origins.
Among the weakest moments of the entire book are chapters 12 and 13, where Chan and Ridley assume the guise of opposing attorneys making final statements to a jury, in favour of “Spillover” and “Accident” respectively. It’s bad because this isn’t a trial; these scenarios aren’t even mutually exclusive; and “Accident” is far from the only alternative to a zoonotic event. If anything, the lab-leak theory is the centrist view, between the benign and sinister extremes of zoonosis and biowarfare. Thus do Chan and Ridley impose an intellectual frame upon the problem that simultaneously blinds readers to the full spectrum of possibility and enfeebles their own position.
But, for all of that, Viral is also a serious and useful book that provides valuable perspective on the recent history of laboratory leaks, which are far more common than almost anyone realises (Chapter 7); the recent history of gain-of-function research (Chapters 8 and 9); the deliberate obfuscations of the World Health Organisation (Chapter 10); and much else besides.
At its core, Viral is an extremely useful compendium of the evidence that the loose Twitter collective known (not altogether fortunately ) as the Decentralised Radical Autonomous Search Team Investigation COVID-19, or DRASTIC, has assembled on the origins of SARS-2. The evidence is rooted above all in the research and strange behaviour of a small group of scientists associated with the Wuhan Institute of Virology, including the so-called bat-woman Shi Zhengli and her close collaborators, Ralph Baric at UNC Chapel Hill and Peter Daszak of the EcoHealth Alliance.
What follows will be less an evaluation of Viral, than a reconsideration of the SARS-2 origins question, on the basis of the evidence that Chan and Ridley assemble. Considering all the clues together in one place has been unexpectedly helpful. In particular, I’ve begun to think about what the DRASTIC evidence actually is, and why the revelations have mostly stopped; how best to interpret the early obfuscations of scientists and Chinese authorities; and finally, what the chronology of their behaviour suggests.
RaTG13 is no longer the closest known relative of SARS-2. It has lost that distinction to BANAL-52, a very slightly closer match which French scientists found in a Malaysian horseshoe bat from Laos in 2020.
This discovery cannot, however, change the historical importance of RaTG13 for understanding the origins of the pandemic. It is at the centre of the case DRASTIC has built for the lab-leak hypothesis, and it is accordingly the very first chapter of Viral.
Here, Ridley and Chan outline all that is known of the Mojiang miners who developed SARS-like symptoms in 2012. Doctors consulted with the WIV on their mysterious illness, and this awakened Shi’s interest in the Mojiang mine, leading to repeated sampling of the horseshoe bats who lived there. According to Shi’s own statements and information released by her lab, RaTG13 was detected in a bat faecal sample collected in 2013, and first sequenced in 2017 and 2018.
Before the pandemic, Shi’s students and others discussed the mine repeatedly in their research, but now they studiously avoid the entire topic, while the mine itself remains closed and under the protection of Chinese security services, who arrest or harass all would-be visitors. In an early paper disclosing the close genetic relationship between SARS-2 and RaTG13, Shi and her colleagues carefully obscured the Mojiang origins of the sequence. Only on the basis of research published prior to 2019 were DRASTIC able to piece the whole story together and force further revelations from the WIV camp.
It has always been very, very hard to accept as mere coincidence, that SARS-CoV-2 first began infecting humans in Wuhan, far from the native habitat of the bats most likely to carry sarbecoviruses like this, but very near indeed to a) a virological institute studying precisely this kind of sarbecovirus, where b) its closest known relative at the time had been sampled and sequenced. If you believe in zoonosis, you have to accept that this natural event purely by accident first came to notice in the one city on earth where this precise variety of virus was the subject of active study and experimentation.
This, then, is what the bulk of the DRASTIC case rests on – a mix of older research, particularly doctoral dissertations, which shed light on the intellectual preoccupations of Shi, her students, and her collaborators; and the more recent, elliptical publications and statements of Shi, Daszak and others at the centre of suspicion. Probably we will not learn very much more; the well of old evidence has gone dry, and nobody from Wuhan or the EcoHealth Alliance is talking anymore.
One question, is why Shi and her associates ever opened their mouths after January 2020 in the first place. Their constant caution and dissimulation is hard to square with what you’d expect of uninvolved researchers, who just happen to find themselves at the centre of a pandemic and are eager to share their insight. On the other hand, wouldn’t we expect clearly implicated parties to destroy evidence and say nothing?
Here I think it’s important to remember that the WIV and the EcoHealth Alliance are civilian research operations. Their programmes are widely known among their academic colleagues, and they involve a lot of technical staff, doctoral students and others. People like Shi are disadvantaged, in that they must address the concerns of two different parties, namely the broader public on the one hand and their own subfield on the other. If they conceal things that other virologists and grantmaking foundations know about, that becomes its own kind of incriminating evidence. This would be why Shi was divulging revealing information about sarbecoviruses from Mojiang in off-hand ways well through December 2020 (see pp. 234-38). The aim would be to get everything that is informally known or suspected into the record in the least damaging way possible. In this they’ve mostly miscalculated, succeeding only in provoking the suspicions of anonymous internet researchers and drawing attention to the very things they wish to hide.
A curious point of Viral, is the degree to which its authors soft-pedal the biological evidence for the unnatural origins of SARS-2. Perhaps they wished to avoid attracting ex-cathedra condemnations of their book from leading avatars of The Science, or perhaps it’s a symptom of their journalistic approach to prize social over scientific evidence. Whatever the case, it’s unfortunate, because the biology of SARS-2 goes a long way to establishing the basic parameters of what might’ve happened in 2019.
I see, at root, three lines of evidence.
The first and weakest is simply that nobody can credibly locate a spillover event or find a natural animal reservoir for SARS-2:
As each month goes by, it becomes more and more extraordinary that the proponents of a natural origin fail to find any of the sort of evidence that very soon came to light in the case of the 2003 SARS epidemic. In that episode it quickly became apparent that food handlers were over-represented in the early cases … Animal traders in Guangdong were found to have antibodies against SARS viruses … [T]he intermediate hosts of the SARS virus were identified within weeks of first sequencing the genome of the virus. (p. 281–82)
SARS is not even the only parallel here; the animal reservoirs of influenza are very obvious and zoonotic infections are often observed. That very few people seem even to be looking for natural SARS-2 reservoirs or trying honestly to identify proximate hosts goes a long way towards suggesting that the laboratory origins of SARS-2 are widely suspected among scientists and government officials. The total lack of interest among Chinese authorities in the earliest Wuhan infections (see esp. pp. 256-58) points very much in the same direction.
A second and stronger line of evidence, highlighted in an early preprint by Alina Chan (also pp. 95–99), is that the virus demonstrated no initial period of rapid adaptation to human hosts. Plainly, by January 2020, SARS-2 was already optimally adapted to infect humans. The precedent of SARS could not be more different. You have to imagine either that we discovered the pandemic very late, and that all that early adaptation happened out of sight; or that SARS-2 experienced a considerable period of early development in a lab, where it had been trained on (repeatedly passaged through) human cell cultures or something like humanised mice.
The third and strongest line of evidence for artificial origins, is the furin cleavage site, subject of a whole chapter in Viral (pp. 202–24). No other sarbecovirus anywhere has been found with this anatomical feature, which plainly enhances the ability of the virus to infect human cells, and which comes complete with ‘optimised’ and (for a sarbecovirus) highly unusual CGG-CGG arginine codons. Furin cleavage sites were a current topic of research within Shi’s circles (p. 208–09), and enhancing sarbecoviruses with these features is even explicitly contemplated in the infamous EcoHealth Alliance grant proposal from 2018 (p. 313). The earliest WIV papers on the SARS-2 genome, from January 2020, moreover appear to specifically avoid discussing this aspect of SARS-2 (p. 221-24). Alas, for Chan and Ridley, “The significance of the S1/S2 furin cleavage site” is characteristically “unclear” (p. 288), while Shi’s puzzling misdirection is moved to centre stage.
The advantage of moving beyond one-dimension “spillover-or-accident” debates, is that we can finally ask what kind of laboratory virus SARS-2 looks to be. Close analogues exist in nature and it’s almost wholly natural. The genome has been lightly tweaked to enhance its ability to infect humans, and otherwise subjected to a process of accelerated adaptation to human hosts in a laboratory.
All of this is entirely consistent with the kind of gain-of-function research we’d expect to have been associated with the USAID ‘Predict’ initiative (see pp. 114–123, pp. 181–97), a post-SARS project aimed at identifying emerging pathogens in animal reservoirs and preventing spillover events. EcoHealth Alliance was of course involved in coordinating Predict and the WIV conducted important research associated with the program.
The dissimulations of Shi, the Chinese authorities and others form the greater part of the case presented in Viral for laboratory origins, and these surely deserve closer study.
There appear to be two distinct clusters of misinformation and obfuscation:
One of these, which we might call the Mojiang Campaign, we’ve already mentioned: This is the consistent dissimulation surrounding bat sampling, virus sequencing and related research undertaken by Shi and her collaborators. Here the information management, at least initially, appears to have proceeded from the scientists themselves, and surrounds everything connected to sarbecoviruses found in the Mojiang mine.
The second locus of dissimulation could be called the Huanan Campaign. It was very likely directed by Chinese public health authorities eager to establish the Huanan Seafood Market as the origin of the Wuhan outbreak. A minor example of this effort would be the early SARS-2 sequence deletions from the National Centre for Biotechnology Information database (p. 54-59), which happened around mid-2020. The purpose seems to have been to hide genetic evidence suggesting that the earliest Chinese infections had no connection to the market and that the Huanan infections were likely secondary. Guilty parties might behave like this, but so might corrupt officials eager to sell a simple origins story reminiscent of SARS to the international press.
Not all of the Huanan Campaign can be explained away in such benign terms, though. Consider the mystery of the pangolins. These are scaly anteating creatures native to Africa and Asia, who were promoted early in 2020 as a likely SARS-2 animal reservoir. Pangolins are prized in China for their scales and their meat, and there is a substantial black market trade. Early in 2020, it was fashionable to argue that the most likely zoonotic source of SARS-2 was pangolins for sale at the Huanan market.
Chan and Ridley, in one of their better chapters (“The Pangolin Papers”: p. 89–106) recount how this myth came to be. The story goes back to seizure by Chinese authorities of smuggled pangolins in March 2019. For unfathomable reasons, Guangdong scientists decided to study 21 of the seized animals for viruses, research that culminated in a very strange October 2019 paper announcing (among other things) that two of them had tested positive for SARS-related coronaviruses.
Sequences of these alleged pangolin sarbecoviruses were then released on 22 January 2020. There followed in February the announcement that the spike protein of one of the these pangolin viruses had a receptor binding domain nearly identical to that of SARS-2. Four separate teams then published papers in February describing SARS-related coronaviruses in pangolins, leading to a flood of media reports. Bizarrely, all of these papers turned out to be nothing but deceptive republications of the same virus sequences from the same pangolin samples first announced in the October 2019 paper.
Chan and Ridley naturally have some concerns about all of this:
[W]e find several things unsettling about the whole pangolin episode. There was the publication of a pangolin coronavirus with such a similar spike receptor-binding domain only a few weeks before the emergence of Covid-19; the release of the pangolin coronavirus data behind the 2019 paper on 22 January 2020, the same day that China announced the Huanan seafood market was the culprit; the posting within three days in February of four manuscripts all describing the same pangolin coronavirus; and the variety of scientific issues plaguing some of these papers’ descriptions of the pangolin coronavirus genome with the SARS-CoV-2-like spike RBD. (p. 105f.)
That is not the half of it. Why the sudden interest in pangolin viruses on the eve of the pandemic in the first place? There’s almost no other research on pangolin viruses at all, and for good reason: As Chan and Ridley note, pangolins are very unlikely to be natural hosts for pathogens like this. Whatever SARS-related viruses those 2019 pangolins were carrying, they had from other animals or from their human smugglers – an obvious conclusion that the October 2019 paper studiously avoids.
It doesn’t take very much conspiratorial mindedness, to say that it looks kind of like evidence for pangolins as the animal reservoir of SARS-2 was planted in the scientific literature all the way back in October 2019, when that first Viruses paper appeared. Then, the researchers sprung the trap, releasing the sequences as part of a coordinated media campaign to establish the Huanan Seafood Market as the proximate origins of SARS-2, while various research teams went on to publish different papers on pangolins as the likely hosts, lending the impression that Chinese researchers had identified close SARS-2 relatives in pangolins multiple times independently.
As for the Mojiang Campaign, here too we find a disturbing foreknowledge.
There is for example the mysterious fate of all the sampling data amassed by Shi and her fellow virologists at the WIV. By 2019 they had apparently assembled twenty-thousand samples, which
were catalogued in a comprehensive 61.5 MB online database, which included nasal and faecal swabs, as well as blood samples from bats and mice. From these were extracted many different virus genetic sequences. A summary paper by the WIV and the EcoHealth Alliance published in 2020 listed 630 novel coronaviruses from samples collected from 2010 to 2015. … [I]n an interview in early December 2019 … Dr Daszak stated: ‘We have now found, after six or seven years of doing this, over a hundred new SARS-related coronaviruses’ … (p. 166)
According to records from a monitoring website, the database went down in the early morning on 12 September 2019, returned “for a few short spells” between December and February” 2020, and then disappeared for good thereafter. The same records “showed a spike of significant activity in June 2019” (p. 168).
A similar picture emerges from the strange obfuscations surrounding what Ridley and Chan call “the other eight” (Chapter 10: pp. 225–243). RaTG13 was not an isolated discovery; it had close relatives that also hail from the Mojiang mine. Shi revealed as much in an embarrassing addendum she was compelled to add to her misleading Nature paper disclosing the affinity between SARS-2 and RaTG13 in February 2020. Some information about these viruses lurked in older research, but it was so opaquely presented that it took anonymous (and not-so-anonymous) internet people months to make sense of it.
The crucial point is this: A 2019 masters thesis co-supervised by Shi provided details on four different sarbecovirus lineages. RaTG13 and its eight Mojiang siblings are the only members of “Lineage 4,” which is also where SARS-2 – had it been known to the masters student – would belong.
The author of the thesis, Yu Ping … published her work in the journal Infection, Genetics and Evolution shortly before she defended her thesis. The paper had been submitted to the journal in November 2018 and published in February 2019. A near replica of the family tree [outlining the four lineages] … from the thesis was published in this mansucript. Except there was no lineage 4. The 2019 journal paper showed only three lineages of SARS-like viruses … There was no discussion of a mine … There was no discussion of an entirely novel group of SARS-like viruses. (p. 242–43).
In other words: When it came time to publish the results, lineage 4, the very lineage comprising SARS-2 and its close Mojiang antecedents, was suppressed.
All the early deception emanating from the Mojiang Campaign, insofar as we can detect it, is of this flavour. Clear information is confined to masters and doctoral theses; key details are kept out of the journals. Researchers routinely downplay the origins of specific samples and identify viruses by an obfuscatory nomenclature. Crucially, though – and whatever the reasons for this anxiety – there’s no outright cover-up until 2020. Even the WIV database was put briefly back online as late as February 2020.
Make of that what you will.
The most powerful objection to lab-leak theory lies in the chronology of the earliest SARS-2 infections. If Corona was already in Italy as early as October 2019, we have to wonder whether Wuhan really was the site of the outbreak. Was Corona just everywhere in Fall 2019, and was Wuhan merely the first place the virus was noticed – or even (to channel Michael P. Senger for a moment) the place where we were first asked to take notice of Corona?
The irony is that the regime narrative is caught between a rock and a hard place here. To make the strongest case for natural origins outside Wuhan requires acknowledging widespread early infection and admitting that lockdowns were worthless. Alternatively, the more the press and the Corona astrologers cleave to the orthodox mythology that Corona did not take off in the West until February 2020, the more they seal the case for a WIV laboratory release.
I’ve thought a lot about this, and I think the balance of evidence lies with Wuhan origins, even if we accept early infections in the West. We probably have to imagine that the virus takes a while to gain momentum and make its way to the least mobile, oldest and sickest people. Before it gets there, nobody will notice anything. Evidence of a novel virus came from Wuhan first, because it was in Wuhan that this novel virus had the biggest head-start.
What is more, pre-Omicron SARS-2 and influenza seem incapable of surging simultaneously in the same population at the same time. Wuhan looks to be the only place that SARS-2 gained a foothold prior to flu season. Thus the Wuhan infections followed a typical influenza trajectory in 2020, while the West saw an abortive spike only after influenza collapsed in March.
No, it still looks very much like something happened in Wuhan in 2019. We just don’t know exactly what that was, or when it happened, or why.
A few additional thoughts at the bottom of this overlong piece:
Sophisticated information-management operations are the province of security and intelligence services, not civilian scientists. The latter advance their careers in the open, by pursuing grant funding, running well-staffed laboratories, training doctoral students and publishing in widely read scientific journals. If SARS-2 were leaked from a civilian laboratory, we’d expect to find evidence of related research programmes in the scientific literature, which is exactly what we do find.
Or rather, it is almost what we find. EcoHealth Alliance and WIV-affiliated theses and publications take us perhaps 80% of the way to SARS-2 origins. That’s far enough to look very bad for them, but you have to ask – where is the rest of that path? Perhaps the missing steps are consistent with an early anxiety surrounding the Mojiang sampling work, which caused researchers to withhold or destroy their latest research well in advance of January 2020. But that isn’t the only possibility, and perhaps it isn’t even the most probable one.
Then there is this: Nobody can have known how SARS-2 – as a lightly enhanced mostly-natural virus that had never spread widely outside its native bat hosts – would behave at large in the human population. Assuming a series of limited experiments or early accidents affecting low-risk military personnel or laboratory staff, researchers might’ve even concluded that the virus was mostly harmless. Certainly, nobody could’ve hoped to cause a pandemic without a sustained campaign of seeding SARS-2, most likely extending across multiple attempts. All of this places serious constraints upon theories of intentional release.