Targeting mitochondria in the infection strategy of the hepatitis C virus

Article ID	Journal	Published Year	Pages	File Type
8324486	The International Journal of Biochemistry & Cell Biology	2013	11 Pages	PDF

Abstract

âº HCV proteins target mitochondria and cause bioenergetic dysfunctions. âº HCV-mediated OXPHOS dysfunctions elicit a pro-surviving adaptation in infected cells. âº A primary and seminal effect of HCV proteins is deregulation of mtCa2+ flux homeostasis. âº A positive feed-back loop between mtCa2+ deregulation and altered redox homeostasis establishes in HCV infected cells. âº Mitochondria-specific drugs prevent and rescue HCV-induced alterations and halt viral replication.

Keywords

RIG-1 RNS GSSG MPTP RyR OXPHOS FFA NAC GSH UPR HIF-1 CARDIF CAT OMM IPS-1 SREBP-1c HCC MAMs N-acetylcysteine ROS ΔμH+Free fatty acid Permeability transition mitochondrial permeability transition pore imm inner mitochondrial membrane Respiratory chain Redox signalling Calcium signalling endoplasmic reticulum hypoxia-inducible factor 1 Mitochondria-associated membranes outer mitochondrial membrane Oxidative phosphorylation caspase activation and recruitment domain SERCA Mitochondria Hepatitis C virus HCV VISA Unfolded protein response Sterol regulatory element-binding protein CARD Hepatocellular carcinoma reduced glutathione oxidised glutathione reactive nitrogen species Reactive oxygen species Ryanodine receptor