Host Cellular Remodeling, Not Viral Transcriptional Inhibition, Drives Quorum Sensing Signal-Mediated Evasion of Viral Lysis in Gephyrocapsa huxleyi
Bacterial infochemicals can profoundly alter phytoplankton physiology, yet how these compounds influence viral infection outcomes remains poorly understood. The bacterial quorum sensing molecule 2-heptyl-4-quinolone (HHQ) enables the globally abundant coccolithophore, Gephyrocapsa huxleyi, to evade virus-induced mortality following infection by Emiliania huxleyi virus (EhV). HHQ reduced infectious virus production at 24 hours despite largely intact viral gene transcription, as revealed by RNA sequencing of host and viral responses during EhV-201 infection. Host transcriptomics instead revealed rapid and progressive HHQ-dependent physiological remodeling evidenced by changes in protein encoding genes associated with vesicular trafficking, and cytoskeletal organization. Transcriptional responses further implicated endolysosomal sorting, membrane remodeling, and protein modification as potential barriers to productive infection. These findings indicate that HHQ-mediated evasion of virus-induced mortality occurs downstream of viral entry and transcription, through remodeling of host processes required for virion assembly, maturation, trafficking, and release.