How do the molecular determinants of antiviral resistance shape the dynamic of phytoplankton-virus interaction?

Phytoplankton sustain all marine ecosystems and are key components of the carbon cycle being responsible for ~50% of the global primary production. A major hypothesis to explain their coexistence with highly efficient lytic viruses is antiviral resistance. Although intracellular and extracellular mechanisms have been shown to underly such resistance and while its determinism is commonly associated to a genomic polymorphism or a (random or virus induced) phenotypic plasticity, comparisons of the impact of those molecular determinants on phytoplankton-virus population dynamic are genuinely lacking. We combined 12 epidemiological models with an unprecedented set of parameter estimates derived from experimental studies of the ubiquitous species Ostreococcus tauri and its prasinoviruses to provide such comprehensive predictions. We show that 'bet-hedging' strategies corresponding to random phenotypic switches between susceptible and resistant cells provide the strongest barrier to virus emergence. When such resistance is associated to intracellular mechanisms the virus' R0 is at least halved because of the strong 'dilution effect' produced by the 'dead-end' hosts. In addition, once the virus has spread, both random and virus-induced phenotypic plasticity strongly stabilize the otherwise 'boom and bust' phytoplankton-virus dynamics, which is highly consistent with the experimental dynamics observed for such interactions.