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Cholesterol and chronic hepatitis C virus infection
Author(s) -
Honda Akira,
Matsuzaki Yasushi
Publication year - 2011
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2011.00838.x
Subject(s) - hypocholesterolemia , cholesterol , medicine , steatosis , ribavirin , hepatitis c virus , hmg coa reductase , lipid metabolism , hepatitis c , endocrinology , pharmacology , reductase , biology , immunology , biochemistry , virus , enzyme
Cholesterol is an essential molecule for the life cycle of the hepatitis C virus (HCV). This review focuses on the roles of cholesterol in HCV infection and introduces HCV events related to cholesterol metabolism and applications for cholesterol metabolism as a therapeutic target. HCV appears to alter host lipid metabolism into its preferable state, which is clinically recognized as steatosis and hypocholesterolemia. While hepatic fatty acid and triglyceride syntheses are upregulated in chronic hepatitis C patients, no direct evidence of increased hepatic de novo cholesterol biosynthesis has been obtained. Impaired VLDL secretion from hepatocytes is suggested to increase intracellular cholesterol concentrations, which may lead to hypocholesterolemia. Clinically, lower serum cholesterol levels are associated with lower rates of sustained virological responses (SVR) to pegylated‐interferon plus ribavirin therapy, but the reason remains unclear. Clinical trials targeting HMG‐CoA reductase, the rate‐limiting enzyme in the cholesterol biosynthetic pathway, are being conducted using statins. Anti‐HCV actions by statins appear to be caused by the inhibition of geranylgeranyl pyrophosphate synthesis rather than their cholesterol lowering effects. Other compounds that block various steps of cholesterol metabolic pathways have also been studied to develop new strategies for the complete eradication of this virus.