Mitochondrial dysfunction in hepatitis C virus infection.
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.
Piccoli
C
C
Department of Biomedical Science, University of Foggia, viale L. Pinto OO.RR. 71100 Foggia, Italy.
Scrima
R
R
D'Aprile
A
A
Ripoli
M
M
Lecce
L
L
Boffoli
D
D
Capitanio
N
N
D015967:Gene Expression Regulation, Viral; D006526:Hepatitis C / Q000473:pathology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology*; D028361:Mitochondrial Diseases / Q000473:pathology* / Q000821:virology*; D014764:Viral Proteins / Q000235:genetics
D014764:Viral Proteins