Carolyn Kormann writes:

Since the coronavirus first appeared, at the end of 2019, four and a half million people have died, countless more have suffered, whole economies have been upended, schools have been shuttered. Why? Did the virus jump from an animal to its first human host, its patient zero? Or, as some suspect, was the catastrophe the result of a laboratory accident in Wuhan, a city of eleven million people in central China?

Kristian Andersen, an infectious-disease expert at Scripps Research, in San Diego, began tracking the virus in January, 2020. He found the degree of contagion not just scary but unusual. Chinese scientists had already established that it belonged to a genus of coronaviruses commonly found in bats in southern China. It shared eighty per cent of its genome with the first SARS, and was more distantly related to MERS, another bat coronavirus. This new virus, however, was spreading far more quickly, reaching at least twenty-six countries by the end of the month. “It seemed to be locked and loaded for causing the pandemic,” Andersen told me. Most viruses circulating in the wild, though some can be deadly, are not very good at transmission. They are still animal viruses. “This, almost from Day One,” Andersen said, “appeared like a human virus.”

Andersen, who is originally from Denmark, is wiry and clean cut, with a cleft chin and clipped enunciation. He was working at the post office in Aarhus when he decided he might study molecular biology, and went on to become the first person in his family to attend university. His career took off with investigations into the emergence of West Nile virus, Ebola, and Zika. After the pandemic began, he was among the scientists whom Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases, consulted regarding the origins of the virus. On January 31, 2020, according to an e-mail obtained by BuzzFeed News, Andersen wrote to Fauci and others that the SARS-CoV-2 genome seemed “inconsistent with expectations from evolutionary theory.”

Andersen noted that “a really small part” of SARS-CoV-2’s genome had “unusual features.” Its spike—the crucial bit of surface protein that a coronavirus uses to invade a cell—appeared able to bind tightly to a human-cell receptor known as ACE2. This, Andersen told me, “means that it’s more effective at infecting human cells.” The other significant trait, a rare insertion in the genome of twelve nucleotides, called a furin cleavage site, might also increase the virus’s transmissibility, and lower the species barrier, allowing the virus to jump more easily to humans. “One has to look really closely at all the sequences to see that some of the features (potentially) look engineered,” he wrote. There was much more data to analyze, he continued, “so those opinions could still change.”

A day later, Andersen joined a conference call with a group of prominent virologists and government officials, including Fauci and Francis Collins, the director of the National Institutes of Health. Andersen presented a summary of the notable features of the SARS-CoV-2 genome, and asked the group, “Do we think this is unusual?” Fauci recalled that, among the participants, opinions were divided. “Knowledgeable people were saying, It does look like it could be something that might be engineered, because it’s not something you usually see,” he told me. “Then you have somebody else equally as knowledgeable say, Oh, nonsense, you can see that in other situations.”

Some comments about the meeting, e-mailed among the group after the call, were redacted. But three days later, on February 4th, Andersen’s perspective shifted. In an e-mail to a different group of scientists, which was recovered by U.S. Right to Know, an investigative group, Andersen wrote, “The main crackpot theories going around at the moment relate to this virus being somehow engineered with intent and that is demonstrably not the case.” [Continue reading…]