Well, there it is. It wasn’t a lab leak after all.

Or was it? Hold that thought.

This news from a new study by European scientists is fascinating — and alarming, since the viruses they harvested in Laos turned out to have receptor binding domains similar to that of SARS-CoV-2. In other words, these viruses evolved naturally to be able to bind to human cells, no lab engineering required. “When SARS-CoV-2 was first sequenced, the receptor binding domain didn’t really look like anything we’d seen before,” said one virologist to the journal Nature. That was part of the reason some scientists believed the coronavirus that causes COVID must have been tinkered with in a lab. These new results undercut that. Mother Nature did the same sort of tinkering via evolution.

Which means a new pandemic could be waiting to happen, just floatin’ around in caves in the Far East as I write this.

Until now, the known virus that most resembled SARS-CoV-2 was called RaTG13 and was discovered in bats in China in 2013. RaTG13 shared 96.1 percent of its genome with the COVID virus, which sounds like a lot but isn’t terribly similar genetically speaking. The viruses found in Laos have gotten us closer to the target:

In an extra step in their study, Eloit and his team showed in the laboratory that the receptor binding domains of these viruses could attach to the ACE2 receptor on human cells as efficiently as some early variants of SARS-CoV-2. The researchers also cultured BANAL-236 in cells, which Eloit says they will now use to study how pathogenic the virus is in animal models.

Last year, researchers described another close relative of SARS-CoV-2, called RaTG13, which was found in bats in Yunnan5. It is 96.1% identical to SARS-CoV-2 overall and the two viruses probably shared a common ancestor 40–70 years ago. BANAL-52 is 96.8% identical to SARS-CoV-2, says Eloit — and all three newly discovered viruses have individual sections that are more similar to sections of SARS CoV-2 than seen in any other viruses.

Viruses swap chunks of RNA with one another through a process called recombination, and one section in BANAL-103 and BANAL-52 could have shared an ancestor with sections of SARS-CoV-2 less than a decade ago, says Spyros Lytras, an evolutionary virologist at the University of Glasgow.

That doesn’t prove where SARS-CoV-2 came from. But the more of its close cousins we encounter in nature, the easier it is to imagine that one of those cousins mutated randomly into the virus that’s killed nearly 700,000 Americans.

But don’t close the book on the lab-leak theory yet. The news yesterday that our old friends at EcoHealth Alliance were looking to tinker with SARS-related bat coronaviruses is more noteworthy today when you realize what the European scientists *didn’t* find in the viruses they harvested in Laos. Although similar to SARS-CoV-2, each one lacked the most distinguishing feature of the virus that causes COVID — the furin cleavage site on the spike protein, which helps the virus bind more efficiently to human cells and makes it unusually transmissible.

The furin cleavage site has been found in other coronaviruses in nature, including at the S1/S2 domain interface. But within the subset of sarbecoviruses, one and only one known to man has a furin cleavage site at that spot. That’s SARS-CoV-2. Despite their genetic similarity to the virus that causes COVID, the sarbecoviruses found in Laos lacked that site. In other words, even close relatives of the virus that causes COVID haven’t acquired its most dangerous advantage. Which raises the question: How did SARS-CoV-2 acquire it?

Read the Intercept’s report on EcoHealth Alliance’s grant proposal to DARPA in 2018. Part of that proposal describes … grafting furin cleavage sites onto the spike proteins of bat coronaviruses.

“Let’s look at the big picture: A novel SARS coronavirus emerges in Wuhan with a novel cleavage site in it. We now have evidence that, in early 2018, they had pitched inserting novel cleavage sites into novel SARS-related viruses in their lab,” said [Alina] Chan. “This definitely tips the scales for me. And I think it should do that for many other scientists too.”

Richard Ebright, a molecular biologist at Rutgers University who has espoused the possibility that SARS-CoV-2 may have originated in a lab, agreed. “The relevance of this is that SARS Cov-2, the pandemic virus, is the only virus in its entire genus of SARS-related coronaviruses that contains a fully functional cleavage site at the S1, S2 junction,” said Ebright, referring to the place where two subunits of the spike protein meet. “And here is a proposal from the beginning of 2018, proposing explicitly to engineer that sequence at that position in chimeric lab-generated coronaviruses.”

Martin Wikelski, a director at the Max Planck Institute of Animal Behavior in Germany, whose work tracking bats and other animals was referenced in the grant application without his knowledge, also said it made him more open to the idea that the pandemic may have its roots in a lab. “The information in the proposal certainly changes my thoughts about a possible origin of SARS-CoV-2,” Wikelski told The Intercept. “In fact, a possible transmission chain is now logically consistent — which it was not before I read the proposal.”

DARPA didn’t give EcoHealth Alliance the funding it was seeking but that doesn’t mean the organization didn’t get it from someone else. And although the proposal suggested most of the genetic tinkering would be done in a U.S. lab in North Carolina, “there is published evidence that the Wuhan Institute of Virology was already engaged in some of the genetic engineering work described in the proposal and that viruses designed in North Carolina could easily be used in China.”

It’s exceedingly strange that EcoHealth Alliance and its leader, Peter Daszak, hadn’t brought this up before now, no?

As a counterpoint to all this, and if you’re willing to wade through scientific jargon, make your way through this paper published last week asserting that the presence of a furin cleavage site on SARS-CoV-2’s spike protein is unlikely to be the product of genetic engineering in a lab. Why? Because there are more efficient such sites found in other viruses than the one found in the COVID virus. If you were a mad scientist splicing together a Frankenstein virus that’s dangerous to humans, wouldn’t you reach for a genetic sequence that’s maximally effective? The sequence in SARS-CoV-2 looks like the sloppy work of Mother Nature recombining genes through random mutation, according to these experts, not the work of laboratory tinkering.