Ecological and evolutionary consequences of viral plasticity

Viruses use the host machinery to replicate, and their performance thus depends on the host’s physiological state. For bacteriophages, this link between host and viral performance has been characterized empirically and with intracellular theories. Such theories are too detailed to be included in models that study host-phage interactions in the long term, which hinders our understanding of systems that range from pathogens infecting gut bacteria to marine phage shaping the oceans. Here, we combined data and models to study the short-and long-term consequences that host physiology has on bacteriophage performance. We compiled data showing the dependence of lytic-phage traits on host growth rate (referred to as viral phenotypic plasticity) to deduce simple expressions that represent such plasticity. Including these expressions in a standard host-phage model allowed us to understand mechanistically how viral plasticity affects emergent evolutionary strategies and the population dynamics associated with different environmental scenarios including, for example, nutrient pulses or host starvation. Moreover, we show that plasticity on the offspring number drives the phage ecological and evolutionary dynamics by reinforcing feedbacks between host, virus, and environment. Standard models neglect viral plasticity, which therefore handicaps their predictive ability in realistic scenarios. Our results highlight the importance of viral plasticity to unravel host-phage interactions and the need of laboratory and field experiments to characterize viral plastic responses across systems.