This means they both have the potential to evolve to become much more damaging to our population.

Coronaviruses have infected every type of vertebrate, from whales and bats to salamanders and snakes. Both influenza and SARS-CoV-2 have huge animal reservoirs. When a virus makes this jump, big things-and often bad things-materialize. But, like influenza, it has also shown itself capable of much more abrupt and substantial changes. One way these major changes happen occurs when a virus jumps to a new population, for example from animals to humans or back again. SARS-CoV-2, like 229E, has already shown that it can drift. But over the past year, our understanding of coronaviruses has improved and we now know that at least one of the cold-causing coronaviruses, designated 229E, undergoes antigenic drift similar to that of influenza. We used to believe that the cold-causing coronaviruses were stable-meaning no antigenic drift-but returned yearly because of faded immune protection. We’ve learned more recently that immunity to influenza also fades, often disappearing within a year, which also makes us susceptible to reinfection. Dominant flu strains evolve from year to year, and the immunity we develop in response to a previous strain has only a muted effect on the new strain. For the flu, antigenic drift-the accumulation of small genetic changes in the virus-has been the primary explanation for recurrent seasonal epidemics. This pattern mimics what we know of cold-causing coronaviruses, which, ever since their discovery in the 1960s, have returned annually to infect us. In the tropics it occurs throughout the year, with only shallow peaks. Influenza, as we know, comes and goes in seasonal waves in the Northern and Southern Hemispheres. Which means influenza’s evolutionary pathway may hold important clues about the road COVID-19 will follow. Indeed, based on what we’ve seen of SARS-CoV-2 and its capacity for variation, I’d say this virus is much more like influenza than any other virus known to date. Other viruses, like influenza, have shown themselves similarly capable of rapid evolution when faced with our best defenses. The doctors and scientists who witnessed their birth called it “accelerated viral evolution.” Under this intense immune pressure, key mutations in the virus emerged. He was undergoing treatment with immunosuppressive drugs when he fell ill, and, during his illness, he received multiple rounds of additional treatment, with remdesivir nonimmune gamma globulin, and with monoclonal antibodies. In Boston, a middle-aged man struggled with a COVID-19 infection for five months before succumbing to the disease. These variants have seemingly been forged in fires of our own making. Since then, multiple new variants have emerged with mutations that can make the virus more transmissible, more lethal and more able to evade our immune defenses. Last summer, a researcher in Texas noticed that a mutated SARS-CoV-2 virus with a substitution in the spike protein had overtaken previous forms to become the dominant strain. Initially, many assumed that coronaviruses in general and SARS-CoV-2 in particular were more stable and less prone to adaptation than other RNA viruses because of their error-proofing mechanisms. For a virus to survive, it must be adapted to its chosen ecological niche-in this case, us-and capable of further intricate adaptation to overcome our best efforts at prevention and treatment. Those that infect humans are faced with an impressive array of defensive weaponry, not just our natural adaptive immunity but also our intelligently designed defenses-vaccines, drugs and social controls. Based on what we know now of SARS-CoV-2, it may no longer be a question of months before an end to the pandemic but a question of years, if not decades. But that rhetoric, in my opinion, is ill-considered and premature. With declining rates of new infections and the rollout of vaccines, some are beginning to speak of an end to COVID-19.

Antigenic shift