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Viruses that infect phytoplankton are abundant in all regions of the global ocean. Despite their ubiquity, little is understood regarding how biotic interactions can alter virus infection success as well as the fate of phytoplankton hosts. In previous work, the bacterially derived compound 2-heptyl-4-quinolone (HHQ) has been shown to protect the cosmopolitan coccolithophoreEmiliania huxleyifrom virus-induced mortality. The present study explores the potential mechanisms through which protection is conferred. Using a suite of transmission electron microscopy and physiological diagnostic staining techniques, we show that whenE. huxleyiis exposed to HHQ, viruses can gain entry into cells but viral replication and release is inhibited. These findings are supported by a smaller burst size, as well as lower infectious and total virus production when the host is treated with nanomolar concentrations of HHQ. Additionally, diagnostic staining results indicate that programmed cell death markers commonly associated with viral infection are not activated when infectedE. huxleyiare exposed to HHQ. Together, these results suggest that the ability of HHQ to inhibit infectious viral production protects the alga not from getting infected, but from cell lysis. This work identifies a new mechanistic role of bacterial quorum sensing molecules in mediating viral infections in marine microbial systems.