‘Escape Mutations’ May Drive New COVID Resurgence

coronavirus cells illustration

Staying home as much as possible and away from other people through the spring could save some 30,000 lives, according to a model from the IHME

The E484K mutation is already causing misery in Manaus, Brazil, a city of 2 million people that sits in the Amazon rainforest.

Brazil, like the U.S., fell short last year in its efforts to ease the COVID-19 crisis. Like former President Donald Trump, Brazilian President Jair Bolsonaro downplayed the risk of the virus, and many people there declined to follow public health recommendations like wearing masks or social distancing.

As a result, Manaus was so hard-hit during its surge of cases last spring that scientists who studied blood samples there estimated that more than 75% of the population might have been infected. As cases dropped over the summer, many wondered whether so many people in Manaus had developed antibodies against the virus that they had achieved some community protection, or herd immunity, against SARS-CoV-2, the virus that causes COVID-19.

The city had not, as it turns out, broken free of COVID.

Cases began to climb again in December, and once again, hospitals were overwhelmed. Some emergency rooms ran out of oxygen, and patients suffocated for lack of treatment.

The second surge baffled researchers and sent them searching for answers. When they looked at the genetic instructions for the coronavirus that was causing the new wave of infections, they could see those blueprints had changed significantly from the original “wild type” virus.

Viruses change all the time. As they copy themselves and jump from host to host, they make mistakes in this copying process, called mutations. Sometimes those mutations give the virus important advantages that help it dominate other forms of the virus.

This new flavor, or variant, of the coronavirus found in Manaus — called P.1 — had 17 key changes, compared to the original.

One of these, the N501Y mutation, is also present in the variant first identified in the U.K., which has made the virus more contagious and caused another surge in cases there. It seems to help the virus bind more easily to doors on our cells called ACE2 receptors.

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