The Roles of Alix and VPS4A in Autophagy and Endosomal Pathways and Their Relation to HBV Replication - PubMed
4 hours ago
- #Autophagy
- #HBV Replication
- #Endosomal Trafficking
- Alix silencing increases intracellular HBV DNA and HBsAg, extracellular HBsAg and virions, while decreasing secreted naked capsids.
- Alix silencing promotes HBsAg secretion via early endosomes but reduces its transport to late endosomes and autophagosomes.
- Alix silencing impairs autophagosome formation by activating the AKT/MTOR pathway.
- VPS4A silencing has minimal effects, but dominant-negative VPS4A blocks HBV secretion by disrupting endosomal trafficking.
- Dominant-negative VPS4A promotes autophagosome formation and lysosome activity, leading to HBV degradation.
- The endosomal pathway is critical for HBV secretion when lysosomal activity is suppressed.
- Increased lysosomal function drives HBV degradation through the autophagosome-lysosome pathway.