Hepatitis C virus hijacks host lipid metabolism.
Hepatitis C virus (HCV) enhances its replication by modulating host cell lipid metabolism. HCV circulates in the blood in association with lipoproteins. HCV infection is associated with enhanced lipogenesis, reduced secretion, and beta-oxidation of lipids. HCV-induced imbalance in lipid homeostasis leads to steatosis. Many lipids are crucial for the virus life cycle, and inhibitors of cholesterol/fatty acid biosynthetic pathways inhibit virus replication, maturation and secretion. HCV negatively modulates the synthesis and secretion of very low-density lipoproteins (VLDL). Components involved in VLDL assembly are also required for HCV morphogenesis/secretion, suggesting that HCV co-opts the VLDL secretory pathway for its own secretion. This review highlights HCV-altered lipid metabolic events that aid the virus life cycle and ultimately promote liver disease.
Department of Medicine, Moores Cancer Center, University of California, San Diego, CA 92093, USA.
Gulam H
GH
Syed
Yutaka
Y
Amako
Aleem
A
Siddiqui
D000818:Animals; D005234:Fatty Liver / Q000209:etiology / Q000503:physiopathology; D016174:Hepacivirus / Q000502:physiology*; D006526:Hepatitis C / Q000378:metabolism* / Q000821:virology*; D019698:Hepatitis C, Chronic / Q000150:complications / Q000378:metabolism / Q000821:virology; D054884:Host-Pathogen Interactions; D006801:Humans; D050356:Lipid Metabolism; D008079:Lipoproteins, VLDL / Q000378:metabolism
D008079:Lipoproteins, VLDL