Academic writing is generally boring. Part of this may be due to the lack of interest in good writing for the sake of writing. Interesting writing can get in the way of the exquisite precision required of the conveyance of scientific information. There is simply no margin for error.
As a writer obliged to interest readers, Katherine Eban may have found herself in a jam, searching for the story hook that would make this palatable to the readers of that most interesting magazine, Vanity Fair. I wish I had a subscription. I wish I were writing for the magazine. Though, if I had written Eban’s article, the editors might not be happy. It would be a little dry. It would lack good guys, bad guys, and infallible Nobel prize winners. It would also lack a writer’s choice of definition. It would provide an as-perfect-as-possible summation, which in this case consists of perfectly balanced uncertainties.
The (CNN) Smerconish interview of Katherine Eban piqued a read of her Vanity Fair article, The Lab-Leak Theory: Inside the Fight to Uncover COVID-19’s Origins.
Up till 1: 10 in the interview, Eban’s statements accurately depict the mainstream of expert opinion, which is: It has so far been impossible to assert or deny a lab leak, which evolved from earlier, strident denial of the lab leak possibility.
After 1:10, there is a digression from the technical, in depiction of cover-your-ass moves and postures that contaminate the lab-leak question. The reporting is credible, but a major distraction from the technical. Barring witness revelations that are unlikely to come from that quarter, this part of Eban’s inquiry is a dead end.
Around 2:33, Eban slips in gain-of-function as a fact of this matter. In doing so, she made a journalist’s choice from a range of informed opinion that spans definitely-not—borderline—definitely-is. She should not be the arbiter of that.
The experiments at WIV were patterned after (Baric, 2015 Naturemedicine) A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence. If this procedure was replicated at WIV, it could not produce COVID-19. If it resulted in general competence that was used in some other way, anything is possible.
For perspective, read (Healthfeedback) What is known about the claims that the Wuhan Institute of Virology conducted research to bioengineer bat coronaviruses? The first thing you should ask yourself is “why the hell should I trust them?” The article quotes the full range of sources on the gain-of-function question, from which Eban picks just one.
A hedgehog is a small animal with quills, but the quills are not as effective against predators as those of a porcupine, which has quills that detach, embedding in the predator, often causing death. Suppose you perform a recombinant genetics experiment that gives a hedgehog the quills of a porcupine. You find that the hedgehog is unable to deploy its quills as effectively as the porcupine. Is this gain of function?
- No, because the hedgehog is not as lethal as the porcupine.
- Yes, because the hedgehog is more lethal than an unmodified hedgehog.
- No, because the intent of the ban is met; hedgehogs are not, and will never become a principal threat.
- Yes, because it is impossible to rule out hedgehogs taking over gardens all over the world.
- Which is it? Not all definitions work as precisely as intended.
A hedgehog with porcupine quills is a chimera, having the parts of several organisms. Baric did this in 2015. WIV continued along these lines, with possible unknown variations, in 2017. Baric’s hedgehog was MA15, a replication-competent, mouse-adapted SARS-CoV backbone. Baric’s porcupine was SHC014 spike.
MA15 could not lead to COVID. Neither could RaTG13. (Healthfeedback) Could scientists use the bat coronavirus RaTG13 to engineer SARS-CoV-2, the virus that causes COVID-19, in a lab?
So what possible unknown variations of procedure at WIV could have included the construction of something approaching the COVID-19 backbone? The literature has so far failed to portray the inability of gene splicing to approach the diversity of mutation in the natural world. It comes down to numbers. Quoting (PMC) The total number and mass of SARS-CoV-2 virions,
Similarly, the arithmetic mean of the number of particles produced over the course of infection of an average individual is 1012–3×1013 viral particles.
As concluded above, about 0.5 mutations are accumulated in every host infection cycle. Without accounting for the effects of selection (i.e. assuming the mutant virions are equally capable of infection and propagation), or the varying chances of mutation among nucleotides,
and for a single, specific, mutation (30,000 are possible),
we expect that such a specific mutation will be observed in one out of every ~200,000 infections.
Every infected human , or animal, is a part of a huge mutation machine, which raises the unlikely above to the realm of events which actually occur. It has been asserted that recombination is limited by the species barrier. This is not true in the natural world, where the synthetically improbable is probable.
Eban refers to (Nicholas Wade, Medium.com ) Origin of Covid — Following the Clues, which is mostly correct, though it falls down on the furin site splicing idea of David Baltimore. Wade quotes David Baltimore, Nobel laureate:
“When I first saw the furin cleavage site in the viral sequence, with its arginine codons, I said to my wife it was the smoking gun for the origin of the virus,” said David Baltimore, an eminent virologist and former president of CalTech. “These features make a powerful challenge to the idea of a natural origin for SARS2,” he said.
Baltimore has since backpedaled, because his reasoning, given in The Debate over Origins of SARS-CoV-2, is factually incorrect. He is a great mind, but mortal. His argument centers on improbability, which I addressed a few paragraphs up. Now for the zinger, the nail in the coffin, from 1992. (Springer, M.M.C. Lai, pdf) Genetic Recombination in RNA Viruses. Quoting page 26,
Besides homologous recombination, some RNA viruses can incorporate either unrelated viral genes or cellular genes into the viral genome, possibly by a nonhomologous recombination mechanism. A characteristic of this type of recombination is that the cellular RNAs or individual viral RNAs involved either do not replicate by themselves or replicate by a mechanism different from that of the RNA virus in question. Therefore, the recombination cannot be explained simply by polymerase jumping from one viral RNA to a different RNA during the course of RNA synthesis. There are several examples of this kind of recombination:
1. Coronavirus MHV contains a HE gene, which was probably derived from influenza C virus by recombination (LUYTJES et al. 1988). These two viruses are unrelated, and the mechanisms of their RNA synthesis are quite different.
This is an example of the power of the natural world to create a viable recombinant virus unlikely to be discovered in the lab. This kind of event occurs in nature, underlying the evolution of new species, such as SARS-COV2.
Does China have a secret? Did WIV diverge from Baric’s methodology? The answer remains infuriatingly beyond our reach. One thing we have on our side, now challenged, is our introspective honesty. Let’s not sacrifice it for the sake of an answer.
Ms. Eban, if you still like me, would you please put me in for a comp subscription? I love the magazine.