Published online Mar 14, 2014. doi: 10.3748/wjg.v20.i10.2624
Revised: November 6, 2013
Accepted: December 12, 2013
Published online: March 14, 2014
Hepatitis C virus (HCV) is the major reason for liver transplantation and the main cause of liver-related morbidity and mortality in a great number of countries. As for the other viruses, this pathogen interferes in more than one process and in more than one way with host cell biology. A mounting body of evidence points, in particular, toward the drastic alterations of mitochondrial physiology and functions that virus is able to induce, albeit the mechanisms have partly remained elusive. Role of the mitochondria in immunity and in quality control systems, as autophagy, as well as the strategies that HCV has evolved to evade and even to manipulate mitochondrial surveillance for its benefit, highlights the importance of deepening the mechanisms that modulate this virus-mitochondrion interaction, not only to intensify our knowledge of the HCV infection pathogenesis but also to design efficient antiviral strategies.
Core tip: Among the strategies that host cells have evolved in the hard fight for their survival against viruses, auto/mitophagy processes have an emerging role. As preferential targets of hepatitis C virus (HCV) attack, mitochondria effectively establish themselves as an integral part of the host cell defense and mitophagy, as very recently unveiled, seriously impacts the course of hepatitis C infection. Aim of this review is to explore the current literature about the mechanisms that regulate the critical interplay between HCV and mitochondria, with particular regard to the strategies that the virus evolved to subvert and manipulate the auto/mitophagy pathways to its purposes.