Reliance of host cholesterol metabolic pathways for the life cycle of hepatitis C virus.
Hepatitis C virus (HCV), a single-stranded positive-sense RNA virus of the Flaviviridae family, infects more than 170 million people worldwide and is the leading cause of liver failure in the United States. A unique feature of HCV is that the viral life cycle depends on cholesterol metabolism in host cells. This review summarizes the cholesterol metabolic pathways that are required for the replication, secretion, and entry of HCV. The potential application of drugs that alter host cholesterol metabolism in treating HCV infection is also discussed.
Ye
Jin
J
Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America. jin.ye@utsouthwestern.edu
D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology; D002784:Cholesterol / Q000378:metabolism*; D016174:Hepacivirus / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D008079:Lipoproteins, VLDL / Q000378:metabolism; D053858:Metabolic Networks and Pathways / Q000187:drug effects / Q000502:physiology*; D008798:Mevalonic Acid / Q000378:metabolism; D012367:RNA, Viral / Q000096:biosynthesis / Q000187:drug effects; D014779:Virus Replication / Q000187:drug effects / Q000502:physiology*