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PubMed · 15758653

Mitochondrial dysfunction in hepatitis C.

Masaaki Korenaga·Michiari Okuda·Kazuhiro Otani·Ting Wang·Yanchun Li·Steven A Weinman
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Abstract

Chronic hepatitis C induces a state of hepatic oxidative stress that is more pronounced than that present in many other inflammatory liver diseases. This review summarizes recent information that the hepatitis C virus (HCV) core protein plays an important role in this phenomenon. Core protein localizes to mitochondria, particularly at the points of contact between mitochondrial outer membrane and endoplasmic reticulum. Its expression causes inhibition of electron transport at complex I, increased complex I reactive oxygen species (ROS) production, decreased mitochondrial glutathione, and increased mitochondrial permeability transition in response to exogenous oxidants and tumor necrosis factor-alpha. Possible mechanisms of the core protein effects include direct interaction with electron carriers and indirect effects mediated by changes in mitochondrial calcium. These results suggest that antioxidant approaches may prove beneficial for patients with chronic hepatitis C.

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HepacivirusHepatitis CHepatitis, AlcoholicHepatocytesHumansMitochondria, LiverOxidative StressReactive Oxygen SpeciesViral Core ProteinsJournal ArticleResearch Support, N.I.H., ExtramuralResearch Support, U.S. Gov't, P.H.S.Review

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Masaaki Korenaga, Michiari Okuda, Kazuhiro Otani, Ting Wang, Yanchun Li, Steven A Weinman. 2005. Mitochondrial dysfunction in hepatitis C.. https://doi.org/10.1097/01.mcg.0000155517.02468.46

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Evaluation of the Abbott RealTime HCV assay for quantitative detection of hepatitis C virus RNA.

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Hepacivirus↗