In recent weeks, concerns have emerged that the use of new antiviral pills, in particular Merck’s molnupiravir, could contribute to this by actively encouraging Sars-CoV-2 to evolve. Molnupiravir works by interfering with the virus’s ability to replicate, littering its genome with mutations until it can no longer reproduce. Some virologists have argued that if any of these viral mutants survive and spread to others, it could theoretically spur the rise of new variants. Others acknowledge that while this is worth monitoring, it is not enough of a concern to deny severely ill patients a potentially lifesaving drug.
Gupta says that a greater problem, and one more likely to lead to a super variant, is the persistently high infection rate in countries such as the UK, due to the ability of Delta to transmit between vaccinated individuals. “The more infections there are per day, the more chance that there is someone out there, a patient X, who gets infected and their T-cells are not strong enough to clear the infection because they’re immune-suppressed,” he says. “So they end up having the infection over a number of days; they’ve got some antibodies knocking around because they’ve had a partial vaccine response and the virus learns to evade them and then that spills out.”
Earlier this year, Gupta published a paper that showed that this process could occur in severely ill patients who had been administered convalescent plasma laden with virus-killing antibodies. Because their immune system still couldn’t clear the virus, it learned to mutate around those antibodies. It has been speculated that the widespread use of convalescent plasma early in the pandemic was responsible for driving the emergence of variants.
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