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Temperate infection in a virus–host system previously known for virulent dynamics

The blooming cosmopolitan coccolithophore Emiliania huxleyi and its viruses (EhVs) are a model for density-dependent virulent dynamics. EhVs commonly exhibit rapid viral reproduction and drive host death in high-density laboratory cultures and mesocosms that simulate blooms. Here we show that this s...

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Detalles Bibliográficos
Autores principales: Knowles, Ben, Bonachela, Juan A., Behrenfeld, Michael J., Bondoc, Karen G., Cael, B. B., Carlson, Craig A., Cieslik, Nick, Diaz, Ben, Fuchs, Heidi L., Graff, Jason R., Grasis, Juris A., Halsey, Kimberly H., Haramaty, Liti, Johns, Christopher T., Natale, Frank, Nissimov, Jozef I., Schieler, Brittany, Thamatrakoln, Kimberlee, Frede Thingstad, T., Våge, Selina, Watkins, Cliff, Westberry, Toby K., Bidle, Kay D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493887/
https://www.ncbi.nlm.nih.gov/pubmed/32934228
http://dx.doi.org/10.1038/s41467-020-18078-4
Descripción
Sumario:The blooming cosmopolitan coccolithophore Emiliania huxleyi and its viruses (EhVs) are a model for density-dependent virulent dynamics. EhVs commonly exhibit rapid viral reproduction and drive host death in high-density laboratory cultures and mesocosms that simulate blooms. Here we show that this system exhibits physiology-dependent temperate dynamics at environmentally relevant E. huxleyi host densities rather than virulent dynamics, with viruses switching from a long-term non-lethal temperate phase in healthy hosts to a lethal lytic stage as host cells become physiologically stressed. Using this system as a model for temperate infection dynamics, we present a template to diagnose temperate infection in other virus–host systems by integrating experimental, theoretical, and environmental approaches. Finding temperate dynamics in such an established virulent host–virus model system indicates that temperateness may be more pervasive than previously considered, and that the role of viruses in bloom formation and decline may be governed by host physiology rather than by host–virus densities.