HCMV US30 induces TMED10-DRP1-mediated mitochondrial fission and apoptosis to promote viral multiplication.
HCMV US30 promotes viral replication by inducing mitochondrial fission and apoptosis through TMED10 and DRP1, with US30-dependent effects accounting for viral dissemination.
- Why it matters: Understanding how HCMV manipulates host cell processes to enhance its replication is crucial for developing targeted therapies against HCMV-related diseases, as the virus hijacks cellular pathways to promote its spread.
- What they did: The study used proteomics and molecular interaction analyses to identify that US30 interacts with NPL4 and TMED10, triggering UPR and mitochondrial fission, respectively, via distinct US30 domains, with US30 altering TMED10 localization to activate DRP1.
- The result: US30-induced mitochondrial fission and apoptosis significantly contribute to HCMV multiplication and dissemination, highlighting potential targets for therapeutic intervention to control HCMV infections.