US missed early chance to slow coronavirus, genetic study indicates

The United States missed out on an early chance to catch imported cases of coronavirus earlier this year, genetics experts say in a new report.

Their analysis of the virus imported by the first person known to have carried the infection to the US — in Washington state back in January — shows it probably was not the source of the later cases there.

And that patient gave the federal government a perfect opportunity to stop further imports, evolutionary biologist Michael Worobey of the University of Arizona and colleagues said.

“Our analyses reveal an extended period of missed opportunity when intensive testing and contact tracing could have prevented SARS-CoV-2 from becoming established in the US and Europe,” they wrote in a report, not yet peer-reviewed and published on the preprint server bioRxiv.

The patient’s story was widely reported. He arrived at Seattle-Tacoma International Airport on January 15, before any health screenings began at US airports.

When the 30-year-old man started feeling symptoms, he remembered warnings from the US Centers for Disease Control and Prevention about the virus and contacted local health officials. He was isolated quickly and Washington state health officials started the process of contact tracing that’s considered the key to containing the spread of infectious disease.

“Everything seemed to have worked the way it was supposed to,” said Joel Wertheim, who teaches at the University of California, San Diego, who worked on the study.

But when more cases turned up in the state at the end of February with no links to new travelers, people started calling the man “patient zero.”

Genetic analysis indicated the virus he was infected with was very similar to viruses that made people ill later. Heath officials couldn’t figure out how the man could have infected other people, but the evidence seemed clear.

But Worobey and colleagues say it turns out the evidence wasn’t so clear.

“Person zero — it never really should have become the thing,” Worobey, a specialist in tracing the lineages of viruses, told CNN. In the study, they call the patient WA1, because he was the first patient in Washington.

Worobey started studying the genetic codes of these viruses, which have been published widely. He saw something odd. Unlike influenza viruses, which mutate almost constantly, this one did not.

“It sort of started to stand out in my mind as an odd pattern,” Worobey said. “I knew what I wanted to do, which was basically to recreate the epidemic in the computer,” he added.

He wanted to model what would have to have happened if patient WA1 really had spread the virus. “With him arriving in January and going out into the community, bumping into other people, and one person transmits to the next and that person transmits to the next and so on until you have thousands of people who are infected,” Worobey said.

He contacted Wertheim, a former graduate student of his, and put together a team of international experts.

They ran simulation after simulation but they all came up with one answer: There was no way the virus that was spreading in Washington state at the end of February was the same version carried in by the traveler on January 15.

There had to have been a second introduction of the virus in mid-February, they concluded. “It looks like early to mid February appears to be the time frame when this virus was introduced to Washington state,” Worobey said.

“It seems that a virus that was probably identical to the Washington epidemic cluster got in at some point in early February and gave rise to a bunch of identical viruses,” Wertheim said.

Where did it come from? Perhaps via Canada. “It seems possible that the virus that eventually wound up in Washington state moved first into Vancouver and then down into Washington,” Worobey said.

“We can’t exactly say when. We can’t say who. We can’t say where from.”

Officials didn’t confirm the first case until January 21 and President Donald Trump said the next day that the virus was “totally under control.” His administration announced it would restrict travel from China on January 31, but restrictions did not take effect until February 2.

The US did not limit travel from Europe until March 11.

“Our finding that the virus associated with the first known transmission network in the US did not enter the country until mid-February is sobering, since it demonstrates that the window of opportunity to block sustained transmission of the virus stretched all the way until that point,” Worobey’s team wrote.

“It is clear that early interventions can have outsized effects on the course of an outbreak,” they added.

The slow mutation rate of the virus makes it hard to track, Worobey said. “It mutates so slowly that there are bound to be lots of times that the virus has moved from one country to another but you can’t distinguish it because it looks like the identical virus. It does get tricky that way,” he said.

“At same time the slow rate of mutation is what allowed it to do what we did here.”

Very tiny differences in the virus that infected the patient in January and the virus infecting people in February were highly significant, he said.

Wertheim, who usually tracks HIV transmission clusters, said the findings are a good example of scientific collaboration and study.

“This is how science is normally done. It is refining and improving our understanding of pandemics,” he said.

But this case was also a lesson in how things can go wrong.

“Erroneously suggesting that WA1 introduced the earliest US outbreak of SARS-CoV-2 obscured the societal and public health benefits produced by an attentive, collaborative, and thoughtful patient willing to work with public health workers to prevent the spread of SARS-CoV-2,” the team wrote.