Lipophagy fuels phosphatidylcholine synthesis for Newcastle disease virus replication - PubMed
12 hours ago
- #Phosphatidylcholine synthesis
- #Newcastle disease virus
- #Lipophagy
- Lipid droplets (LDs) serve as dynamic organelles storing neutral lipids and maintaining lipid homeostasis.
- Newcastle disease virus (NDV) exploits LDs via SQSTM1/p62-dependent lipophagy to selectively degrade triglycerides (TAGs) rich in unsaturated fatty acids (UFAs).
- NDV infection leads to depletion of UFA-containing triglycerides (UFA-TAGs) and UFA-containing phosphatidylcholines (UFA-PCs).
- Inhibition of lipophagy blocks LD degradation, reduces viral replication, and suppresses UFA-PC formation.
- Lipophagy-derived UFAs are incorporated into phosphatidylcholines (PCs) via the Kennedy pathway, not β-oxidation.
- UFA supplementation rescues viral replication under lipophagy blockade and promotes virus-like particle (VLP) release.
- NDV links lipophagy-driven UFA release to phospholipid synthesis and membrane remodeling, revealing a metabolic vulnerability for antiviral strategies.