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MicroRNAs and hepatitis C virus: Toward the end of miR-122 supremacy

Thomas Walter Hoffmann12, Duverlie Gilles123 and Bengrine Abderrahmane13*

Author Affiliations

1 EA4294 Unité de Virologie Clinique et Fondamentale, Université de Picardie Jules Verne, UFR de Médecine et de Pharmacie, 3 rue des Louvels, 80036, Amiens Cedex, France

2 Laboratoire de Virologie, Centre Hospitalier Universitaire d’Amiens, Avenue René Laennec, 80480, Salouël, France

3 Biobanque de Picardie, Centre Hospitalier Universitaire d’Amiens, Avenue René Laennec, 80480, Salouël, France

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Virology Journal 2012, 9:109  doi:10.1186/1743-422X-9-109

Published: 12 June 2012


The most common etiologic agents causing chronic hepatitis are hepatitis C and B viruses (HCV and HBV, respectively). Chronic infection caused by HCV is considered one of the major causative agents of liver cirrhosis and hepatocellular carcinoma worldwide. In combination with the increasing rate of new HCV infections, the lack of a current vaccine and/or an effective treatment for this virus continues to be a major public health challenge. The development of new treatments requires a better understanding of the virus and its interaction with the different components of the host cell. MicroRNAs (miRNAs) are small non-coding RNAs functioning as negative regulators of gene expression and represent an interesting lead to study HCV infection and to identify new therapeutic targets. Until now, microRNA-122 (miR-122) and its implication in HCV infection have been the focus of different published studies and reviews. Here we will review recent advances in the relationship between HCV infection and miRNAs, showing that some of them emerge in publications as challengers against the supremacy of miR-122.

MicroRNAs; Hepatitis C virus; Virus-host interactions; New therapeutic targets