When You Eliminate the Impossible

Speaking of articulating arguments in an op-ed in the Wall Street Journal Steven Quay and Richard Muller argue that the science supports the lab-leak hypothesis for the origin of SARS-CoV-2. Here’s the first part of their argument which I don’t find particularly convincing:

Although the double CGG is suppressed naturally, the opposite is true in laboratory work. The insertion sequence of choice is the double CGG. That’s because it is readily available and convenient, and scientists have a great deal of experience inserting it. An additional advantage of the double CGG sequence compared with the other 35 possible choices: It creates a useful beacon that permits the scientists to track the insertion in the laboratory.

Now the damning fact. It was this exact sequence that appears in CoV-2. Proponents of zoonotic origin must explain why the novel coronavirus, when it mutated or recombined, happened to pick its least favorite combination, the double CGG. Why did it replicate the choice the lab’s gain-of-function researchers would have made?

The problem is that unlikely even remarkably improbable things happen all of the time. Here’s the second part of their argument:

There is additional scientific evidence that points to CoV-2’s gain-of-function origin. The most compelling is the dramatic differences in the genetic diversity of CoV-2, compared with the coronaviruses responsible for SARS and MERS.

Both of those were confirmed to have a natural origin; the viruses evolved rapidly as they spread through the human population, until the most contagious forms dominated. Covid-19 didn’t work that way. It appeared in humans already adapted into an extremely contagious version. No serious viral “improvement” took place until a minor variation occurred many months later in England.

Such early optimization is unprecedented, and it suggests a long period of adaptation that predated its public spread. Science knows of only one way that could be achieved: simulated natural evolution, growing the virus on human cells until the optimum is achieved. That is precisely what is done in gain-of-function research. Mice that are genetically modified to have the same coronavirus receptor as humans, called “humanized mice,” are repeatedly exposed to the virus to encourage adaptation.

which I find a lot more convincing. Here’s their conclusion:

The presence of the double CGG sequence is strong evidence of gene splicing, and the absence of diversity in the public outbreak suggests gain-of-function acceleration. The scientific evidence points to the conclusion that the virus was developed in a laboratory.

I’m surprised that they didn’t mention what is to me the more convincing evidence: that in the hundreds of thousands of animal samples tested nothing particularly close to SARS-CoV-2 has been identified. As I’ve pointed out before the similarity between SARS-CoV-2 and the closest bat virus they’ve identified as potential relatives is more like the difference between a human and a cat than it is like the difference between a human and a chimp let alone the genetic similarity between two different humans. Evolution just doesn’t work that way.