There are three possible explanations for why the evolution of SARS-CoV-2 looks so different from that of other viruses, and they are not mutually exclusive. First of all, we really haven’t looked that hard at other respiratory viruses. More than 7.5 million genomes of SARS-CoV-2 have been sequenced; just a few hundred or a few dozen for each of the four seasonal coronaviruses have been. When scientists try to reconstruct the relationship among these sequenced viruses in evolutionary trees, “the trees are so sparse,” says Sarah Cobey, a biologist at the University of Chicago. A whole suite of other viruses also cause common colds: rhinoviruses, adenoviruses, parainfluenza, respiratory syncytial virus, metapneumovirus, and so on. These, too, are poorly sampled. More than 100 types of rhinoviruses alone infect humans, but we don’t have a great understanding of how that diversity came to be or evolved over time.

Second, the coronavirus could indeed be an outlier that is inherently better than other viruses at exploring its fitness landscape. “It helps to be an RNA virus”—which acquires mutations more quickly than a DNA virus—“and then it helps to be moving really fast,” Cobey told me. Measles takes, on average, 11 or 12 days between infecting one person and that person infecting another; the coronavirus takes only 1.5 to three. The more people it can infect, the more of the fitness landscape it can explore.

Third, the coronavirus was a novel pathogen. Whatever intrinsic transmissibility it may have had, it was also unimpeded by immunity when it first arrived in the human population.