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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 28, 2015; 21(28): 8492-8507
Published online Jul 28, 2015. doi: 10.3748/wjg.v21.i28.8492
Hepatitis C virus comes for dinner: How the hepatitis C virus interferes with autophagy
Daniela Ploen, Eberhard Hildt
Daniela Ploen, Eberhard Hildt, Paul-Ehrlich-Institut, Department of Virology, 63225 Langen, Germany
Eberhard Hildt, Deutsches Zentrum für Infektionsforschung, 38124 Braunschweig, Germany
Author contributions: Ploen D and Hildt E analyzed the literature and wrote the manuscript.
Conflict-of-interest statement: The authors have no conflict of interest to report.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Eberhard Hildt, Paul-Ehrlich-Institut, Department of Virology, Paul-Ehrlich-Street 51-59, 63225 Langen, Germany. eberhard.hildt@pei.de
Telephone: +49-6103-772140 Fax: +49-6103-771273
Received: March 3, 2015
Peer-review started: March 5, 2015
First decision: April 29, 2015
Revised: May 10, 2015
Accepted: June 15, 2015
Article in press: June 16, 2015
Published online: July 28, 2015
Abstract

Autophagy is a highly-regulated, conserved cellular process for the degradation of intracellular components in lysosomes to maintain the energetic balance of the cell. It is a pro-survival mechanism that plays an important role during development, differentiation, apoptosis, ageing and innate and adaptive immune response. Besides, autophagy has been described to be involved in the development of various human diseases, e.g., chronic liver diseases and the development of hepatocellular carcinoma. The hepatitis C virus (HCV) is a major cause of chronic liver diseases. It has recently been described that HCV, like other RNA viruses, hijacks the autophagic machinery to improve its replication. However, the mechanisms underlying its activation are conflicting. HCV replication and assembly occurs at the so-called membranous web that consists of lipid droplets and rearranged endoplasmic reticulum-derived membranes including single-, double- and multi-membrane vesicles. The double-membrane vesicles have been identified to contain NS3, NS5A, viral RNA and the autophagosomal marker microtubule-associated protein 1 light chain 3, corroborating the involvement of the autophagic pathway in the HCV life-cycle. In this review, we will highlight the crosstalk of the autophagosomal compartment with different steps of the HCV life-cycle and address its implications on favoring the survival of infected hepatocytes.

Keywords: Hepatitis C virus, Hepatitis, Autophagy, Morphogenesis, Replication

Core tip: The hepatitis C virus (HCV) is the major cause of chronic liver disease worldwide. According to the world health organization, approximately 130-170 million people are chronically infected with HCV. It has recently been described that HCV hijacks the autophagosomal pathway. Autophagy is a conserved cellular process that catabolizes intracellular components to maintain cellular homeostasis. Besides, autophagy is involved in the development of human diseases. In this review, we will depict the data known so far, corresponding the interplay between the autophagosomal pathway and the different steps of the HCV life-cycle.