Abstract

Viruses replicate and evolve within the hosts that they infect, but sooner or later they need to transmit if they are going to survive in the long term. This creates an evolutionary trade-off, because what makes a virus fit within a given individual does not necessarily make it good at transmitting. We might expect this tension to be strongest for chronic viral infections, like HIV , which can undergo years of rapid within-host evolution between transmission events. But for acute viruses, like SARS CoV-2, these tensions are expected to be weak as the virus rapidly jumps from individual to individual, with little opportunity for within-host selection. This is supported out by ours’ and others’ findings that when viral loads are high and transmission is most likely, SARS -CoV-2 has little genetic diversity and a narrow transmission bottleneck. How then does the appearance and success of new variants of concern, which apparently emerged within chronically infected individuals, fit into this framework? I argue that by changing the properties of the host population, for example as a consequence of host shifts or mass vaccination, we are fundamentally changing the nature of the trade-off between selection at the within and between-host levels. I will finish with a brief discussion on what this might mean for modelling SARS -CoV-2 viral dynamics in the context of viral evolution in the future.