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Joffe, N.

Publications and source records attributed to Joffe, N..

2 recordsLinked to original sources

Reversible inhibition of viral life cycle in response to elevated temperature in a bloom-forming alga

Ocean warming is expected to reshape microbial interactions and community composition, with profound consequences for marine biogeochemical cycles. Host-virus dynamics are central to these processes, yet their response to elevated temperature remains poorly understood. Here, using the bloom-forming alga Gephyrocapsa huxleyi and its specific large dsDNA virus, Emiliania huxleyi virus (EhV), we show that elevated temperature withheld virion production and abolished distinct stages of the viral life cycle. Viral adsorption and early transcription remained active, whereas viral DNA replication and late gene expression were arrested, leading to an intracellular inhibition of infection. Intriguingly, this arrested infection state was reversible following prolonged heatwave conditions. Single-cell analyses revealed that reversibility of infection inhibition occurred both within a small fraction of infected cells and by reinfection by extracellular virions that remained viable during heat exposure in the extracellular milieu. Furthermore, we detected variability in infection inhibition by temperature across several host-virus pairs, suggesting that the effect of temperature is strain-specific. Our findings uncover a temperature-sensitive checkpoint in the viral life cycle, providing a mechanistic framework for understanding how marine heatwaves may reshape virus-driven mortality and carbon cycling in the ocean.

microbiology↗

Cell-to-cell heterogeneity drives host-virus coexistence in a bloom-forming alga

Algal blooms drive global biogeochemical cycles of key nutrients in the oceans and serve as hotspots for biological interactions. The massive spring blooms of the cosmopolitan coccolithophore Emiliania huxleyi (E. huxleyi) are often infected by the lytic Emiliania huxleyi specific virus (EhV) which is a major mortality agent triggering bloom demise. Nonetheless, the multi-annual "boom and bust" pattern of E. huxleyi suggests that mechanisms of coexistence are essential for these host-virus dynamics. To investigate host-virus coexistence, we developed a new model system from an E. huxleyi culture which recovered from viral infection. The recovered population coexists with the virus, as host cells continue to grow in parallel to viral production. By applying a single-molecule fluorescence in situ hybridization (smFISH) approach to quantify the fraction of infected cells and assessing infection-specific lipid biomarkers, we identified a small subpopulation (5-7% of cells) that was infected and produced new virions, whereas the majority of the host population could resist infection. To further assess population heterogeneity, we generated monoclonal strain collections using single-cell sorting and subsequently phenotyped their susceptibility to EhV infection. This unraveled a substantial cell-to-cell heterogeneity across a continuum of susceptibility to resistance, suggesting that infection outcomes may vary depending on the individual cell. These results add a new dimension to our understanding of the complexity of host-virus interactions that are commonly assessed in bulk and described by binary definitions of resistance or susceptibility. We propose that phenotypic heterogeneity drives E. huxleyi-EhV coexistence and may potentially provide the coexisting strain an ecological advantage by killing competing susceptible strains.

microbiology↗