Mitochondrial dysfunction in hepatitis C virus infection

C. Piccoli, R. Scrima, A. D'Aprile, M. Ripoli, L. Lecce, D. Boffoli, N. Capitanio

Research output: Contribution to journalArticlepeer-review

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 mtΔΨ, 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.

Original languageEnglish
Pages (from-to)1429-1437
Number of pages9
JournalBiochimica et Biophysica Acta - Bioenergetics
Volume1757
Issue number9-10
DOIs
Publication statusPublished - Sep 2006

Keywords

  • Calcium
  • Complex I
  • Endoplasmic reticulum
  • HCV
  • Inducible gene expression
  • Mitochondria
  • Reactive oxygen specie

ASJC Scopus subject areas

  • Biophysics

Fingerprint

Dive into the research topics of 'Mitochondrial dysfunction in hepatitis C virus infection'. Together they form a unique fingerprint.

Cite this