Herpes Simplex Virus 1 (HSV-1) Uses the Rab6 Post-Golgi Secretory Pathway For Viral Egress
Melissa H Bergeman1,2, Kimberly Velarde2, Honor L Glenn3
1ASU-Banner Neurodegenerative Disease Research Center, Arizona State University.
Biorxiv : the Preprint Server for Biology
|January 3, 2024
Summary
Herpes Simplex Virus 1 (HSV-1) utilizes the host
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Herpes Simplex Virus 1 (HSV-1) infects a majority of the global population, yet its intracellular transport and exocytosis mechanisms remain unclear.
- Understanding these late stages of HSV-1 replication is crucial for developing targeted antiviral therapies.
Approach:
- Developed a live-cell fluorescence microscopy assay to track individual HSV-1 particles during intracellular trafficking and exocytosis.
- Utilized a pH-sensitive reporter to pinpoint the exact moment and location of particle exocytosis.
- Investigated the role of host cell factors, specifically the Rab6 GTPase, in HSV-1 egress.
Key Points:
- HSV-1 particles colocalize with the host Rab6 protein in the Golgi region.
- HSV-1 virions traffic with Rab6-containing vesicles to the cell periphery.
- Exocytosis of HSV-1 occurs via Rab6-mediated secretory vesicles.
Conclusions:
- HSV-1 egress utilizes the host's pre-existing Rab6 post-Golgi secretory pathway.
- This pathway mediates the polarized egress of HSV-1 from infected cells.
- HSV-1 egress does not rely on novel, virus-induced mechanisms but rather hijacks cellular machinery.
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