Mitochondrial dysfunction in hepatitis C virus infection

作者：Piccoli C; Scrima R; D'Aprile A; Ripoli M; Lecce L; Boffoli D; Capitanio N^*

来源：Biochimica et Biophysica Acta-Bioenergetics, 2006, 1757(9-10): 1429-1437.

DOI：10.1016/j.bbabio.2006.05.018

• HCV
• inducible gene expression
• mitochondria
• reactive oxygen specie
• complex I
• endoplasmic reticulum
• calcium

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 mt Delta psi, 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.

• 出版日期2006-10