The problem with molnupiravir lies in its mechanism of action. Unlike any previous antiviral drug, molnupiravir does only one thing: It introduces mutations into the viral genome. We are already familiar with the fact that viruses naturally mutate to evade immunity; the many mutations of the spike protein in omicron, for example, allow it to evade the antibodies created by prior infections or vaccines. Molnupiravir relies on inducing even more mutations so that eventually the virus’s proteins are damaged beyond function. That molnupiravir can mutate SARS-CoV-2 to death has been demonstrated in the controlled conditions of a petri dish and lab animal cages, leading Merck to test it in covid-19 patients in clinical trials…

The first days of molnupiravir treatment present a clear opportunity for mutant viruses to be transmitted to family members or caregivers. Viral evolution is a process of selecting for rare mutations that are beneficial to the virus. It doesn’t matter if just one out of the billions of copies of viruses in an infected individual mutates to a higher level of fitness. That single copy, either by evading existing antibodies or replicating to yet higher levels of fitness, will become amplified either in that patient or in the next person infected.

The worst-case scenario is worrisome. As long as molnupiravir is in use somewhere in the world, it could generate repeated cycles of new variants, with people desperately taking the drug to fight the new variants it spawns, creating a vicious positive feedback loop while causing more suffering and deaths.