Targeting mitochondria in the infection strategy of the hepatitis C virus

Giovanni Quarato, Rosella Scrima, Francesca Agriesti, Darius Moradpour, Nazzareno Capitanio, Claudia Piccoli

Research output: Contribution to journalArticle


Hepatitis C virus (HCV) infection induces a state of oxidative stress more pronounced than that observed in many other inflammatory diseases. Here, we propose a temporal sequence of events in the HCV-infected cell whereby the primary alteration consists of a release of Ca2+ from the endoplasmic reticulum, followed by uptake into mitochondria. This ensues successive mitochondrial dysfunction leading to the generation of reactive oxygen species and a progressive metabolic adaptive response. Evidence is provided for a positive feed-back mechanism between alterations of calcium and redox homeostasis. This likely involves deregulation of the mitochondrial permeability transition and induces progressive dysfunction of cellular bioenergetics. Pathogenetic implications of the model and new opportunities for therapeutic intervention are discussed. This article is part of a Directed Issue entitled: Bioenergetic dysfunction, adaptation and therapy.

Original languageEnglish
Pages (from-to)156-166
Number of pages11
JournalInternational Journal of Biochemistry and Cell Biology
Issue number1
Publication statusPublished - Jan 2013


  • Calcium signalling
  • Hepatitis C virus
  • Mitochondria
  • Permeability transition
  • Redox signalling

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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