As others more competent than I to judge have noted elsewhere, the last few months have brought a sea change in the media coverage on the origins of the COVID-19 pandemic. The previously-stigmatized "lab leak hypothesis" has gained increased credibility among politicians, journalists, and some scientists, though it also continues to have its vocal critics. As a layperson with minimal understanding of genetics or infectious disease, I feel unequipped to address the scientific issues at the center of the controversy. I will state, however, that an excellent recent write-up of the available evidence by Zeynep Tufekci in the New York Times has convinced me of at least one thing: there are more options available to us than the simple binary form of the question (was it a lab leak? or not?) often leads us to believe.
As I understand from reading Tufekci's article, speaking of "the lab leak hypothesis" in the singular is somewhat of a misnomer; we really are talking about a cluster of different possibilities. I propose we divide these in two: the "strong" and the "weak" versions of the lab leak hypothesis. The strong holds that the SARS-CoV-2 virus was engineered in a lab—most likely one housed in the Wuhan Institute of Virology (WIV) or the Wuhan Centers for Disease Control and Prevention (CDC)—through gain-of-function research. The weak version, by contrast, is agnostic on the question of whether SARS-CoV-2 was created through human genetic tampering or evolved via natural selection; it posits merely that the virus—however it came into being—was stored in one of these facilities and accidentally escaped, causing the first detectable human outbreak.
Based on Tufekci's summary of the findings to date, it seems the strong version of the hypothesis is implausible at this point; and it is chiefly against this version alone that the strongest scientific firepower has hitherto been directed. Tufekci recapitulates the chief arguments that have been raised against it by Kristian Andersen and others. These boil down—as I understand them—to two main points. First: the other sequenced bat coronavirus known to be in the WIV lab is not genetically similar enough to SARS-CoV-2 for it to have changed into the latter, either through deliberate gain-of-function manipulation or natural evolution. Second: there are aspects of the structure of SARS-CoV-2's spike proteins that we would not expect to see, if it really had been developed through gain-of-function testing.
Convincing as these points may be, however, it is worth noting that neither touches the weak version of the hypothesis. This, as we have seen, is fully compatible with the theory that SARS-CoV-2 evolved in nature—among a reservoir of bats in the wild, most likely; it simply hypothesizes the virus was then brought into a lab and accidentally released thence to the public, perhaps by well-intentioned researchers who had taken it with them precisely because they had been looking for the type of bat coronavirus that might prove virulent in humans (in order to aid efforts to stop future pandemics).
This latter form of the theory not only has not been debunked; there is also circumstantial evidence in its favor. I would summarize this as follows, based on Tufekci's article: 1) no animal has so far been identified that might have served as an intermediate link in the transmission chain between bats and humans, as would be expected under the most common form of the zoonotic hypothesis; this suggests that SARS-CoV-2 may have evolved to allow for direct bat-to-human transmission; 2) there is no substantial wild bat population near Wuhan, but the city is home to laboratories that are among the few in the world actively engaged in bat coronavirus research; 3) interview and video evidence indicates that researchers affiliated with WIV and Wuhan CDC engaged in field research with bats, at times without adequate safety precautions, and may have stored live bats on site in Wuhan.
From this, a coherent and plausible hypothesis (though it remains only that) emerges that researchers may have acquired the virus on a research expedition, bringing it back themselves as asymptomatic carriers or in a bat colony they housed in the lab, whence it escaped into the public. This is not an idle fear, since such breaches of lab safety are relatively common throughout the world (not just in China) and have been linked to disease outbreaks before—including a relatively minor eruption of SARS that killed one person in 2005 and a global flu pandemic in 1977 that was most likely caused by frozen samples of an older flu virus stored in a lab. The scenario in which scientific and medical researchers have created the very monster they set out to prevent, making COVID-19 in part at least iatrogenic in origin, is thus a very real and disturbing possibility.
If it could in fact be shown that the catastrophic global toll of COVID-19 was due in part to insufficient safeguards taken at some of the labs handling bat coronaviruses (and it's worth emphasizing again here that is still a big "if"), we might be tempted to see in this the stuff of promethean tragedy: the hubris of modern scientific probing into nature's domain, punished at last by the nemesis of pandemic disease. Disciples of Ivan Illich, say, could scarcely hope for a more dramatic and horrifying confirmation of their prior distrust of modern technological interventions in health. But before we go further down that path, it is worth pointing out how much any epidemic represents an upset of the natural order. Scientific research is far from the only or the most damaging way in which humans tamper with our environment, that is to say, in ways that cause disease.
This insight was borne home for me this past week by reading William McNeill's classic study Plagues and Peoples. The author reminds us epidemic disease is by no means a normal or a lasting condition under most natural conditions, because in most settings, given enough time, a sort of equilibrium nearly always obtains between host and parasite. The microbial organisms that cause disease in humans, after all, face extinction as much as we do if they kill off their hosts too readily. It is to their advantage to allow for the continued existence of the animals in which they take up residence; and thus, over a prolonged period, a pathogen and a host will tend to produce a lasting interrelationship that allows for their mutual (if not always entirely symbiotic) coexistence.
This situation typically only changes when either: 1) humans encounter a totally new pathogen for which they have no inherited immunity, oftentimes as a result of human societies penetrating a natural environment they had not previously entered; or 2) a pathogen that usually makes its home in a different animal species, with whom it has established an equilibrium, makes the jump to human-to-human transmissibility as a result of an unusual degree of contact with people.
The latter seems to be what happened in the case of SARS-CoV-2, whether one prefers the zoonotic hypothesis or the weak form of the lab leak theory. These animal-to-human transfers, as we have seen, are more likely to happen when humans are penetrating a new environment and encountering and handling a wild species with which they would seldom have come into contact under ordinary circumstances. Thus, they could take place as a result of scientific field work. But they could just as easily come about through the trapping of wild animals for sale in a wet market, the hunting of bushmeat, the destruction of habitats and resulting displacement of wild animals through clearing forests to make way for pastureland, etc.—all likely pathways for pandemic disease that Mike Davis warned us about as early as 2005, in his book The Monster at Our Door.
The question of how this particular pandemic came about is very important, and we should investigate every likely avenue; but my point is that even if it should turn out that it originated from a lab, the policy conclusions as to what we should do going forward, to prevent the next pandemic, remain largely unchanged, whether we accept the zoonotic or the weak lab leak hypothesis. In either case, the lesson should not be to restrict science or research, but rather to take stronger steps to limit the intrusion of human beings on such a large scale into previously undisturbed natural environments and the habitats of wild animals with whom we do not typically come into contact.
This can be accomplished—as Mike Davis noted well over a decade ago—by limiting the overfishing and consumption of resources by companies based in rich countries, whose practices interfere with the food sources of subsistence producers in the Global South, forcing many of them to turn to bushmeat to survive. It can be done through preventing right-wing authoritarians like Brazil's Jair Bolsonaro from fulfilling their threats to undermine Indigenous land rights and carve up Native people's sovereign territory for the sake of clearing more ground for cattle grazing—which happens to be a major threat to the climate and the Earth's biodiversity, by the way, in addition to heightening all of humanity's risk of exposure to pandemic.
In short, the possibility that scientists may have unwittingly unleashed pandemic disease upon us—through invading a wild bat habitat without appropriate safeguards—is not a lesson about the perils of science and medicine so much as a warning about the risks of any interference with what Burns called "nature's social union." It is by disturbing this union, by introducing disequilibria into carefully-calibrated natural balances between hosts and microscopic parasites, evolved over millennia, that —according to McNeill's account—all epidemics come about. The experience of the COVID-19 crisis should therefore inform not only how we approach our research methods and lab safety, but how we treat the entire ecology that forms the backdrop for human life. "O if we but knew what we do/When we delve or hew," Gerard Manley Hopkins once wrote, surveying a landscape of downed trees. His implied answer: we might think better of it.
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