Before becoming a Covid-19 drug, each candidate was just a tiny fragment of someone’s immune system, part of a swarm of Y-shaped proteins unleashed to try to keep the coronavirus from invading more cells. If the person recovered, these antibodies might end up in a blood sample in a lab. Some proved more effective than others. Yet even as researchers pinpointed the best of the bunch as possible medications, they knew their power could wane: What worked against the coronavirus as it was last year could falter as the pathogen evolved.
That’s starting to play out, in that some monoclonal antibodies now used to treat patients in the U.S. aren’t great at gumming up the machinery of some new SARS-2 variants. But scientists are betting that those same Darwinian patterns that nudged the virus to become less susceptible to certain treatments can be used to our advantage as well, guiding ongoing development efforts.