The two antivirals are slightly different agents of chaos, though. To make more of itself, SARS-CoV-2 deploys a scribe-like enzyme called a polymerase to scan and duplicate its genome letter by letter. When the polymerase spots a stray remdesivir molecule, it stumbles, as if flustered by a bad typo. Molnupiravir is more insidious still. It’s such a good mime of the letters in the viral alphabet that the polymerase often overlooks the interloper, making genome copies riddled with mistakes. “An analogy might be gross misspellings,” Painter said. The drug’s sabotage is so extensive that experts call it an “error catastrophe”: Dangerous viral particles have essentially no shot of emerging out the other end.

Molnupiravir’s packaging might give it another leg up. Researchers have long known that a bad case of COVID-19 tends to unfurl in two stages—one dominated by the virus, and a second by the immune system’s overzealous reaction. The point of antivirals is to act early, and fast—to nip a growing virus population in the bud, before it can wreak havoc on our tissues, or trip too many of the body’s hypersensitive alarms. These drugs are largely useless once people have descended into the second phase. Remdesivir has to be delivered intravenously, over several days—usually in a hospital, after most patients are pretty sick. (This might explain why remdesivir studies in these settings have produced mixed or underwhelming results.) Molnupiravir, meanwhile, was designed as a pill so it could be “easily administered in the outpatient setting,” Daria Hazuda, Merck’s vice president of infectious disease and vaccine discovery, told me. The drug is easily shipped and stored, and can be taken pretty much anywhere.