California scientists have discovered a home-grown coronavirus strain that appears to be spreading faster than any other variant on the loose in the Golden State.
Two independent research groups said they found the new strain while looking for signs that a highly transmissible variant from the UK had settled here. Instead, they found a new branch of the virus’s family tree – the one whose sudden appearance and distinct mutations made him the prime suspect in California’s violent vacation boom.
As they studied genetic sequencing data in late December and early January, the two teams saw evidence of the proliferation of the new strain jumping from their spreadsheets. Although focused on different regions of the state, they found trends that were strikingly similar and deeply worrying.
Researchers at Cedars-Sinai Medical Center in Los Angeles found that, although the strain was almost imperceptible in early October, it was responsible for 24% of the approximately 4,500 viral samples collected across California in the last weeks of 2020.
In a separate analysis of 332 virus samples taken mainly from northern California during late November and December, 25% were of the same type.
“There was a home grown variant under our noses,” said Dr. Charles Chiu, a laboratory medicine specialist at UC San Francisco who examined samples from the northern part of the state with collaborators from the California Department of Public Health. If they weren’t looking for the UK strain and other viral variants, he said, “we could have missed it at all levels”.
The new strain, which scientists dubbed B.1.426, has five mutations in its genetic code. One, known as L452R, changes the virus’s spike protein, the tool it uses to infiltrate human cells and turn them into virus factories.
Over several generations, even a small improvement in this ability will help a virus to spread more easily through the population, increasing infections, hospitalizations and deaths.
One-off surveillance efforts that use genetic sequencing to track changes in the virus detected a single instance of B.1.426 in California in July. As far as scientists can tell, he was down for the next three months.
Then it got busy.
The Cedars-Sinai team collected 192 viral samples from patients at the medical center between 22 November and 28 December. At 11 pm on New Year’s Eve, they loaded these samples into their genetic sequencer, which began spitting out the data. the first weekend of the new year. The sudden prominence of the tension aroused admiration and sadness.
“We said, ‘Wow! There’s something different, something we didn’t expect to find, ‘”said Dr. Eric Vail, a pathologist who usually sequences genes in search of cancer drivers. “Suddenly, your brain starts racing at an hourly rate.”
All thoughts quickly turned to the disastrous increase in COVID-19 in the state – an increase in illness and death that pushed hospitals to the limit, killed more than 18,000 Californians and doubled the total death toll in the state in less than three months.
Did they find the culprit?
The preliminary evidence looked damning. It was certainly found at the crime scene. Confused health workers working to contain the outbreak raised the hypothesis that they were facing a new strain of coronavirus with improved transmission capacity.
But there were several other suspects to be considered as well, including cold weather, restaurant dinners, holiday gatherings and a growing disregard for public health measures.
To clarify B.1.426’s role in the sudden increase, researchers will need to determine how much devastation it is capable of producing. This investigation will focus on its transmissibility, as well as its ability to bypass the tools – including masks, drugs and vaccines – that can be used to control the pandemic.
For now, the two groups of researchers doubt that they have found a single actor. But they may have caught an accomplice.
Chiu said his skepticism stems in part from the fact that the increase in cases across the state appears to have started before the new strain reached its most marked growth. “It may have contributed to this increase, or it simply contributed to the ride,” he said.
In addition, the sudden prominence of the strain among viral samples in northern California may be due in part to its role in an unusually large outbreak at Kaiser Permanente San Jose Medical Center that infected at least 77 employees and 15 patients, and resulted in death of an employee. Authorities are investigating whether an infected but asymptomatic employee managed to spread the virus widely with the help of a battery-powered fan that was part of an inflatable Christmas tree costume.
“It seemed to spread very fast,” said Dr. Sara Cody, health officer for Santa Clara County, where the hospital is located. “Are we trying to understand if the characteristics of this outbreak are because of this variant – this variant of the virus behaves in a different way – or does it have to do with other factors that were present in the hospital?”
In Southern California, where the wave timelines and the emergence of B.1.426 seem more aligned, researchers are more inclined to blame the virus.
“It probably helped to speed up the number of cases during the holiday season,” said Vail. “But human behavior is the predominant factor in the spread of a virus, and the fact that it happened when the weather cooled and in the middle of the holidays, when people got together, is not an accident.
Scientists at Chiu’s laboratory have already started to cultivate armies of the new strain, derived from four patients recently infected with it. The creation of large batches under controlled conditions is the first step in testing whether any of its mutations increases its ability to grab, invade and hijack human cells.
These initial efforts raised concerns.
“It grows quite robustly,” said Chiu.
Adding to his concern are the findings of other Howard University researchers who developed and tested a version of the coronavirus with the L452R mutation, which gained prominence in a strain that emerged in Denmark in March. Howard’s team found that the mutation helps the virus to bind more tightly to human cells, enhancing their transmission.
In Chiu’s laboratory, as well as Cedars-Sinai, scientists will test the new strain to look for signs that B.1.426 mutations have improved its performance.
Other experiments will explore whether antibodies generated by the immune system of people who have been infected or vaccinated against the coronavirus will recognize this new strain.
Some overwhelming evidence has already come to light. State health officials reported this week that a patient in Monterey County who tested positive for an infection in April and has now recovered has been infected with B.1.426.
This suggests that the new strain may be able to hide its presence of antibodies created after exposure to other versions of the virus – a phenomenon known as “immune escape”. If so, it can impair the effectiveness of COVID-19 vaccines and antibody-based treatments.
“The bottom line is that this is a variant that is becoming more prevalent and we need to lean over and understand more about it,” said Cody.