African swine fever virus hijacks lipolysis induced by chaperone-mediated autophagy to upregulate fatty acid β-oxidation and promote viral replication - PubMed
4 days ago
- #African swine fever virus
- #lipid metabolism
- #viral replication
- African swine fever virus (ASFV) manipulates host lipid metabolism to enhance viral replication.
- ASFV infection upregulates both fatty acid synthesis (FAS) and fatty acid β-oxidation (FAO).
- Inhibition of FAS or FAO impairs ASFV replication.
- ASFV alters lipid droplet (LD) composition, promoting viral replication.
- ASFV induces chaperone-mediated autophagy (CMA) to degrade perilipin 2 (PLIN2), stimulating lipolysis.
- ASFV infection triggers LD-mitochondrion contacts, facilitating fatty acid transfer for FAO.
- The study reveals a complex metabolic network involving FAS, LD biogenesis, lipolysis, and FAO in ASFV replication.
- Findings suggest potential therapeutic targets by modulating lipid metabolism to inhibit ASFV.