Document Detail


Activation of unfolded protein response and autophagy during HCV infection modulates innate immune response.
MedLine Citation:
PMID:  21723841     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
Autophagy, a process for catabolizing cytoplasmic components, has been implicated in the modulation of interactions between RNA viruses and their host. However, the mechanism underlying the functional role of autophagy in the viral life cycle still remains unclear. Hepatitis C virus (HCV) is a single-stranded, positive-sense, membrane-enveloped RNA virus that can cause chronic liver disease. Here we report that HCV induces the unfolded protein response (UPR), which in turn activates the autophagic pathway to promote HCV RNA replication in human hepatoma cells. Further analysis revealed that the entire autophagic process through to complete autolysosome maturation was required to promote HCV RNA replication and that it did so by suppressing innate antiviral immunity. Gene silencing or activation of the UPR-autophagy pathway activated or repressed, respectively, IFN-β activation mediated by an HCV-derived pathogen-associated molecular pattern (PAMP). Similar results were achieved with a PAMP derived from Dengue virus (DEV), indicating that HCV and DEV may both exploit the UPR-autophagy pathway to escape the innate immune response. Taken together, these results not only define the physiological significance of HCV-induced autophagy, but also shed light on the knowledge of host cellular responses upon HCV infection as well as on exploration of therapeutic targets for controlling HCV infection.
Authors:
Emilie Estrabaud; Simon De Muynck; Tarik Asselah
Publication Detail:
Type:  Comment; Journal Article     Date:  2011-07-01
Journal Detail:
Title:  Journal of hepatology     Volume:  55     ISSN:  1600-0641     ISO Abbreviation:  J. Hepatol.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-10-19     Completed Date:  2012-03-06     Revised Date:  2012-08-24    
Medline Journal Info:
Nlm Unique ID:  8503886     Medline TA:  J Hepatol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1150-3     Citation Subset:  -    
Copyright Information:
Copyright © 2011 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
Affiliation:
Service d'Hépatologie and INSERM U773 CRB3, Beaujon Hospital, University Paris VII, France.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Comments/Corrections
Comment On:
J Clin Invest. 2011 Jan;121(1):37-56   [PMID:  21135505 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Lifestyle interventions for the treatment of non-alcoholic fatty liver disease in adults: a systemat...
Next Document:  Resveratrol triggers the pro-apoptotic endoplasmic reticulum stress response and represses pro-survi...