How do the molecular determinants of antiviral resistance shape the dynamic of phytoplankton-virus interaction?
Abstract
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.
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BibTeX
@misc{rousseau2026molecular,
title = {{How do the molecular determinants of antiviral resistance shape the dynamic of phytoplankton-virus interaction?}},
author = {Raphaël Rousseau and Carlos Cáceres and Gwenaël Piganeau and Sébastien Gourbière},
howpublished = {HAL},
year = {2026},
month = sep,
doi = {10.64898/2026.09.29.755341},
url = {https://hal.science/hal-05777816v1},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - UNPB
TI - How do the molecular determinants of antiviral resistance shape the dynamic of phytoplankton-virus interaction?
AU - Raphaël Rousseau
AU - Carlos Cáceres
AU - Gwenaël Piganeau
AU - Sébastien Gourbière
PY - 2026
DA - 2026/09/29
PB - HAL
DO - 10.64898/2026.09.29.755341
UR - https://hal.science/hal-05777816v1
AB - 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.
ER -