To explore the impact of these two mutations, the researchers introduced them—both together and separately—into SARS-CoV-2 cultured in a lab dish. Viruses with the D796H mutation or with both mutations were better at evading antibodies, suggesting that antibodies exerted “pressure” to generate mutations. The D796H mutation alone made the virus worse at infecting cells. The ∆H69/∆V70 deletion alone, however, made the virus twice as efficient at infecting cells—a hallmark of B.1.1.7. Virus with both mutations infected cells similarly to the original unmutated population, suggesting the two mutations canceled one another out when it came to infectiousness. The analysis showed that the D796H mutation arose first, and Gupta postulates that the deletion may have arisen in response. “It’s as if the virus was trying to fix itself,” he says, by making up for the infectivity deficit.
Rapid evolution of the virus has been documented in other patients as well, including a Boston man hospitalized at Brigham and Women’s Hospital, which was reported December 3 in the New England Journal of Medicine. Jonathan Li, a virologist and an author of that case study, says his group also found multiple mutations, but they didn’t understand the implications until later. Once those same mutations were described in B.1.1.7 and other variants and were found to change the virus’s behavior, “that’s when we realized [it] was a harbinger of what’s to come.”
