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Mitochondrial dysfunction in hepatitis C virus infection.

C Piccoli·R Scrima·A D'Aprile·M Ripoli·L Lecce·D Boffoli·N Capitanio
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Abstract

The mechanisms of liver injury in chronic hepatitis C virus (HCV) infection are poorly understood though HCV induces a state of hepatic oxidative stress that is more pronounced than that present in many other inflammatory diseases. This mini-review will focus on recent findings revealing an unexpected role of mitochondria in providing a central role in the innate immunity and in addition will illustrate the application of stably transfected human-derived cell lines, inducibly expressing the entire HCV open reading frame for in vitro studies on mitochondria. Results obtained by a comparative analysis of the respiratory chain complexes activities along with mitochondrial morpho-functional confocal microscopy imaging show a detrimental effect of HCV proteins on the cell oxidative metabolism with specific inhibition of complex I activity, decrease of mtDeltaPsi, increased production of reactive oxygen species. A possible de-regulation of calcium recycling between the endoplasmic reticulum and the mitochondrial network is discussed to provide new insights in the pathogenesis of hepatitis C.

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Gene Expression Regulation, ViralHepatitis CHumansImmunity, InnateMitochondriaMitochondrial DiseasesViral ProteinsJournal ArticleReview

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C Piccoli, R Scrima, A D'Aprile, M Ripoli, L Lecce, D Boffoli, N Capitanio. 2006-05-19. Mitochondrial dysfunction in hepatitis C virus infection.. https://doi.org/10.1016/j.bbabio.2006.05.018

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