Abstract
•A model is used to explore the stability and dynamics of a host-virus system.•In our model, viral traits depend on host physiology (viral plasticity).•Including viral plasticity promotes coexistence between the virus and its host.•Host-virus coexistence may occur as steady states or oscillatory solutions.•Viral plasticity usually damps oscillations, but may amplify them in certain cases.
Phenotypic plasticity plays an important role in the survival of individuals. In microbial host-virus systems, previous studies have shown the stabilizing effect that host plasticity has on the coexistence of the system. By contrast, it remains uncertain how the dependence of the virus on the metabolism of the host (i.e. “viral plasticity”) shapes bacteria-phage population dynamics in general, or the stability of the system in particular. Moreover, bacteria-phage models that do not consider viral plasticity are now recognised as overly simplistic. For these reasons, here we focus on the effect of viral plasticity on the stability of the system under different environmental conditions. We compared the predictions from a standard bacteria-phage model, which neglects plasticity, with those of a modification that includes viral plasticity. We investigated under which conditions viral plasticity promotes coexistence, with or without oscillatory dynamics. Our analysis shows that including viral plasticity reveals coexistence in regions of the parameter space where models without plasticity predict a collapse of the system. We also show that viral plasticity tends to reduce population oscillations, although this stabilizing effect is not consistently observed across environmental conditions: plasticity may instead reinforce dynamic feedbacks between the host, the virus, and the environment, which leads to wider oscillations. Our results contribute to a deeper understanding of the dynamic control of bacteriophage on host populations observed in nature.