Cargando…

Hepatitis C Virus-Induced Mitochondrial Dysfunctions

Chronic hepatitis C is characterized by metabolic disorders and a microenvironment in the liver dominated by oxidative stress, inflammation and regeneration processes that lead in the long term to hepatocellular carcinoma. Many lines of evidence suggest that mitochondrial dysfunctions, including mod...

Descripción completa

Detalles Bibliográficos
Autores principales: Brault, Charlène, Levy, Pierre L., Bartosch, Birke
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705306/
https://www.ncbi.nlm.nih.gov/pubmed/23518579
http://dx.doi.org/10.3390/v5030954
_version_ 1782476414346330112
author Brault, Charlène
Levy, Pierre L.
Bartosch, Birke
author_facet Brault, Charlène
Levy, Pierre L.
Bartosch, Birke
author_sort Brault, Charlène
collection PubMed
description Chronic hepatitis C is characterized by metabolic disorders and a microenvironment in the liver dominated by oxidative stress, inflammation and regeneration processes that lead in the long term to hepatocellular carcinoma. Many lines of evidence suggest that mitochondrial dysfunctions, including modification of metabolic fluxes, generation and elimination of oxidative stress, Ca(2+) signaling and apoptosis, play a central role in these processes. However, how these dysfunctions are induced by the virus and whether they play a role in disease progression and neoplastic transformation remains to be determined. Most in vitro studies performed so far have shown that several of the hepatitis C virus (HCV) proteins localize to mitochondria, but the consequences of these interactions on mitochondrial functions remain contradictory, probably due to the use of artificial expression and replication systems. In vivo studies are hampered by the fact that innate and adaptive immune responses will overlay mitochondrial dysfunctions induced directly in the hepatocyte by HCV. Thus, the molecular aspects underlying HCV-induced mitochondrial dysfunctions and their roles in viral replication and the associated pathology need yet to be confirmed in the context of productively replicating virus and physiologically relevant in vitro and in vivo model systems.
format Online
Article
Text
id pubmed-3705306
institution National Center for Biotechnology Information
language English
publishDate 2013
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-37053062013-07-09 Hepatitis C Virus-Induced Mitochondrial Dysfunctions Brault, Charlène Levy, Pierre L. Bartosch, Birke Viruses Review Chronic hepatitis C is characterized by metabolic disorders and a microenvironment in the liver dominated by oxidative stress, inflammation and regeneration processes that lead in the long term to hepatocellular carcinoma. Many lines of evidence suggest that mitochondrial dysfunctions, including modification of metabolic fluxes, generation and elimination of oxidative stress, Ca(2+) signaling and apoptosis, play a central role in these processes. However, how these dysfunctions are induced by the virus and whether they play a role in disease progression and neoplastic transformation remains to be determined. Most in vitro studies performed so far have shown that several of the hepatitis C virus (HCV) proteins localize to mitochondria, but the consequences of these interactions on mitochondrial functions remain contradictory, probably due to the use of artificial expression and replication systems. In vivo studies are hampered by the fact that innate and adaptive immune responses will overlay mitochondrial dysfunctions induced directly in the hepatocyte by HCV. Thus, the molecular aspects underlying HCV-induced mitochondrial dysfunctions and their roles in viral replication and the associated pathology need yet to be confirmed in the context of productively replicating virus and physiologically relevant in vitro and in vivo model systems. MDPI 2013-03-21 /pmc/articles/PMC3705306/ /pubmed/23518579 http://dx.doi.org/10.3390/v5030954 Text en © 2013 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Brault, Charlène
Levy, Pierre L.
Bartosch, Birke
Hepatitis C Virus-Induced Mitochondrial Dysfunctions
title Hepatitis C Virus-Induced Mitochondrial Dysfunctions
title_full Hepatitis C Virus-Induced Mitochondrial Dysfunctions
title_fullStr Hepatitis C Virus-Induced Mitochondrial Dysfunctions
title_full_unstemmed Hepatitis C Virus-Induced Mitochondrial Dysfunctions
title_short Hepatitis C Virus-Induced Mitochondrial Dysfunctions
title_sort hepatitis c virus-induced mitochondrial dysfunctions
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705306/
https://www.ncbi.nlm.nih.gov/pubmed/23518579
http://dx.doi.org/10.3390/v5030954
work_keys_str_mv AT braultcharlene hepatitiscvirusinducedmitochondrialdysfunctions
AT levypierrel hepatitiscvirusinducedmitochondrialdysfunctions
AT bartoschbirke hepatitiscvirusinducedmitochondrialdysfunctions