Viruses infect host cells to hijack the host machinery for viral reproduction, which can lead to host mortality for unicellular organisms. In marine environments, viruses are recognized as an important factor altering phytoplankton and bacterioplankton growth and dynamics. However, it is still unclear the exact role that viruses play in the regulation of their host populations. As a consequence, generalizing viral-mediated processes is still a big challenge in ecology as well as in other fields (e.g. medical or commercial, where viruses are suggested as an alternative to antibiotics for humans, plants, or animals).Lab experiments reveal that viral performance (represented by infection time and offspring number) varies with physiological changes in their hosts, effectively the virus' environment. These variations are referred as viral phenotypic plasticity, as the viral traits vary when environmental conditions change. In the past, models studying viral plasticity focused on intracellular dynamics. However, these latter are too detailed to be included in models that study host-virus population-level interactions in the long term, which hinders our understanding of systems that range from pathogens infecting gut bacteria to marine phage shaping the ocean communitiesHere, we compiled experimental data to represent lytic viral plasticity through functional forms that are biologically meaningful, and which we included in a standard host-virus model to understand the effect of viral plasticity on (i) the evolutionary response of the viral traits as well as population dynamics, (ii) the persistence of the host-virus systems, and (iii) the coevolution between host and virus. We show that the plasticity of the viral offspring number mostly drives the phage ecological and evolutionary dynamics. Moreover, plasticity can invert predictions on the short-term population dynamics of the viral-host system made by classic models that neglect viral plasticity.Considering viral plasticity leads to a dynamic viral control of the host population, and enables coexistence in region where classic (nonplastic) models predict the collapse of the population. Finally, the coevolution of host-phage populations shows beneficial mutualistic interactions where the presence of virus, instead of having a negative effect, increases the fitness of the host.
|Date of Award||16 Jun 2020|
- University Of Strathclyde
|Sponsors||University of Strathclyde|
|Supervisor||Mike Heath (Supervisor) & Juan Bonachela (Supervisor)|