It is a theory that seems to be spreading as quickly as the virus itself:
The new coronavirusis infecting relatively few in California because the state suffered a silent outbreak as far back as the fall, well before official reports indicate it hit the U.S. As a result, the theory goes, many residents are now resistant to the disease.
The hypothesis, sparked by an article written for the conservative National Review by a military historian affiliated with Stanford University, went viral in recent weeks. Questions around when and how quickly the virus began to spread resurfaced Tuesday, after authorities in the San Francisco Bay Area reported that the first U.S. death from the virus took place in one of its counties on Feb. 6—nearly three weeks earlier than previously reported.
The theory, that the first U.S. cases could have occurred undetected months earlier, has been used to support arguments that social distancing, as being practiced in California and many other places, might be unnecessary.
The first diagnosed case in the U.S. was on Jan. 21 in Washington state, according to the Centers for Disease Control and Prevention. Scientists say there is no scientific evidence to indicate the virus was circulating last year. They point to testing on patients with respiratory symptoms on the West Coast that revealed very few cases even in February, and note the genetic blueprint of the virus hadn’t significantly mutated in February and March, based on studies of samples from patients in California. Viruses tend to mutate over time.
Recent studies indicate that while the number of infections is likely greatly underreported, nowhere near enough Californians are infected to generate the kind of vast herd immunity required to damp the virus.
“Any talk about the virus circulating in the fall has no scientific evidence,” said Charles Chiu, an infectious-diseases expert at the University of California, San Francisco.
Viruses mutate as they infect more people, gradually straying from their original blueprint. To test whether the novel coronavirus was newly introduced to California, or had been circulating there for a long time, Dr. Chiu examined the genomes of a number of local cases.
Dr. Chiu mapped several known strains of the virus in the 29 people who tested positive in Northern California between Feb. 3 and March 15. “Early infections disproportionately occurred in returning travelers,” he said.
The strain circulating aboard the Grand Princess cruise ship that docked in Oakland matched the first known U.S. infection in January. Two individuals from the same household in San Mateo County matched a strain from China. And other individuals from the same county matched strains circulating in Europe. Dr. Chiu’s research is being peer-reviewed.
In a separate study that hasn’t yet been reviewed, Dr. Chiu found 20 of the first 46 patients diagnosed at UCSF had traveled to places such as Europe and New York, among other U.S. cities. That dovetails with other research that found that early infections detected in California closely resemble strains earlier reported elsewhere, suggesting visiting or returning travelers introduced the infection rather than that it was circulating over time.
To examine the early spread of Covid-19—the disease caused by the virus—in the San Francisco Bay Area, researchers tested nasopharyngeal samples collected from people between Jan. 1 and Feb. 26. Those people sought care for respiratory problems at Stanford Health Care but tested negative for common respiratory viruses. Of the 2,888 patients screened, only two tested positive for Covid-19.
“Our results suggest that viral prevalence in the Bay Area was low before February,” said Benjamin Pinsky, medical director of Stanford’s clinical virology laboratory, whose findings were vetted by other experts and published in the Journal of the American Medical Association earlier this month.
A similar study of more than 6,900 people who reported flu-like symptoms in Seattle earlier this year detected its first Covid-19 infection in late February.
Doctors testing for antibodies, which show whether an individual was previously infected, do say the number of U.S. infections is grossly underestimated. Earlier this month, researchers estimated that 2.8% to 5.6% of Los Angeles County’s 10 million adults had been infected at some point.
Those numbers, however, are nowhere close to the levels typically needed for herd immunity of 50% or above, said Michael Busch, director of the Vitalant Research Institute, which is conducting a nationwide serology study funded by the National Institutes of Health. “I doubt we’ll see more than 5% to 10% of the U.S. population immune,” Dr. Busch said.
Victor Davis Hanson, the author of the National Review article, said in a follow-up piece dated April 11 that he didn’t claim to be a “doctor, much less an epidemiologist or a conductor of any such study,” and that he wasn’t affiliated with Stanford’s medical school.
In an email, Mr. Hanson added, “We are in a completely fluid situation, more of the certainties of the last 5 weeks have been proven uncertain and we should entertain an open mind about the next patient zero, the likely number of infected, the lethality of the virus,” as well as “the track record of ‘not likely’ or ‘likely’ assessments.”
His theory lives on. In a series of tweets last week, conservative radio-show host Bill Mitchell pushed the idea of herd immunity to his hundreds of thousands of followers. “The downside of social distancing, assuming it works at all, is that it prevents herd immunity,” he wrote.
San Francisco interior designer Susan Collins spied the theory on
Twitter. Now she believes her dry cough in December means she is one of the many Californians who has already contracted, and recovered from, coronavirus.
“I’m convinced I had it,” she said. “A ton of people are out there saying the virus has been around for much longer than we think. It’s totally believable.”
