The news of infections caused by a novel coronavirus, and the everyday use of the names SARS-CoV-2 and COVID-19, became widespread around February. But, the question of how long the virus had already been present in the United States before that time has remained unknown. Now, a team of researchers has reconstructed some of the early transmissions of the virus. By analyzing the genomic sequences of SARS-CoV-2 samples from infected patients in Washington State, they suggest that most early SARS-CoV-2 infections derive from a single introduction in late January or early February, sparking rapid community transmission of the virus that went undetected for several weeks before this community spread became evident.
This work is published in Science in the paper, “Cryptic transmission of SARS-CoV-2 in Washington State.”
The team, led by Trevor Bedford, PhD, associate professor in the vaccine and infectious disease division at the Fred Hutch, and colleagues at the University of Washington in Seattle, analyzed genetic sequences of 453 SARS-CoV-2 genomes from the Washington State outbreak collected between January 19 and March 15.
The first confirmed case of SARS-CoV-2 in the United States was identified in Washington State on January 19 in an individual returning from Wuhan. The team’s genomic analysis revealed that 84% of the genomes in their study fall into a closely related group to the first case. This group is called the Washington State outbreak clade and derives from viruses circulating in China. The authors wrote that the Washington State outbreak clade has a highly “comb-like” structure, indicative of rapid exponential growth.
The findings also suggest that most of the early SARS-CoV-2 cases in the state came from a single introduction of the virus, probably between January 22 and February 10.
The first case of community spread was detected on February 28. To better understand the transmission chain that led to it, Bedford and colleagues analyzed more than 10,000 specimens collected as part of the Seattle Flu Study between January 1 and March 15. They found evidence for SARS-CoV-2 a few days before the first previously reported community case in Washington. Refining the time and geographic origin of the introduction into Washington State will require a combination of earlier samples and samples from other geographic locations, the authors said.
They also noted that other states in the United States have shown different genetic histories from Washington State, with a majority of SARS-CoV-2 sequences from New York and Connecticut clustering within European lineages, for example.
In addition to the 384 viruses from Washington State identified in the Washington State outbreak clade, they observed 12 viruses from elsewhere, including California, Connecticut, Minnesota, New York, North Carolina, Virginia, Utah, Australia, and the Grand Princess cruise ship.
The authors wrote that in January and February, screening for SARS-CoV-2 in the United States was directed at travelers with fever, cough, and shortness of breath, with point of origin broadening as new outbreaks were identified, but specifying travel to China up until February 24. Their analysis indicates that at least one clade of SARS-CoV-2 had been circulating in the Seattle area for 3–6 weeks by the time the virus was first detected in a non-traveler on February 28. By then, variants within this clade constituted the majority of confirmed infections in the region (84%). Several factors could have contributed to the delayed detection of presumptive community spread, including limited testing among non-travelers or the presence of asymptomatic or mild illnesses.
Their results highlight the critical need for widespread surveillance for community transmission of SARS-CoV-2, even after the pandemic is brought under control, said the authors. They noted that several factors could have contributed to the delayed detection of presumptive community spread in Washington, including limited testing among non-travelers.
