Epidemiological model selection unravels the molecular processes of antiviral resistance from experimental phytoplankton-virus dynamics

Phytoplankton-virus interactions are pivotal in understanding the intertwined dynamics of these key players of the global carbon cycle. Although antiviral resistance is the main hypothesis to solve the apparent paradox of their coexistence, identifying its molecular determinisms and mechanisms, as well as their dynamical consequences, remains challenging. By combining hypotheses about such determinisms and mechanisms, we designed 36 dynamical models and fitted them to experimental infection kinetics in a pioneering selection model approach. Through such a multiple hypotheses testing, we identified that resistance in the model species Ostreococcus tauri is most likely to be predominantly intracellular, to control lysis through budding, and to be acquired by phenotypic plasticity. We further showed that viral kinetics are strongly impacted by both the antiviral resistance′s molecular determinants and virions′ inactivation through attachment to lysis detritus, as the latter generates a key negative feedback loop during the ′bust′ stage of the interaction dynamics.