Journal of Hepatology
Volume 51, Issue 3 , Pages 606-609, September 2009

Unravelling the importance of microRNAs during hepatitis C virus infection in the human liver☆

  • Sébastien Pfeffer

      Affiliations

    • Architecture et Réactivité de l’ARN, Université de Strasbourg, Institut de biologie moléculaire et cellulaire du CNRS, 15 rue René Descartes, 67084 Strasbourg Cedex, France
    • Corresponding Author InformationCorresponding authors. Tel.: +33 3 88417060; fax: +33 3 88602218 (S. Pfeffer), Tel.: +33 3 90243703; fax: +33 3 90243710 (T.F. Baumert).
    • ,
  • Thomas F. Baumert

      Affiliations

    • Unité Inserm U748, Université de Strasbourg, 3 rue Koeberlé, 67000 Strasbourg, France
    • Service d’Hépatogastroentérologie, Nouvel Hôpital Civil, 1 Place de l’Hôpital, 67091 Strasbourg Cedex, France
    • Corresponding Author InformationCorresponding authors. Tel.: +33 3 88417060; fax: +33 3 88602218 (S. Pfeffer), Tel.: +33 3 90243703; fax: +33 3 90243710 (T.F. Baumert).

published online 28 April 2009.

Special Section Editors: Peter R. Galle, Peter L.M. Jansen, Francesco Negro

Decreased levels of microRNA miR-122 in individuals with hepatitis C responding poorly to interferon therapy. Sarasin-Filipowicz M, Krol J, Markiewicz I, Heim MH, Filipowicz W.

Several microRNAs (miRNAs), including liver-specific miR-122, have been implicated in the control of hepatitis C virus (HCV) RNA replication and its response to interferon (IFN) in human hepatoma cells. Our analysis of liver biopsies from subjects with chronic hepatitis C (CHC) undergoing IFN therapy revealed no correlation of miR-122 expression with viral load and markedly decreased pretreatment miR-122 levels in subjects who had no virological response during later IFN therapy; other investigated miRNAs showed only limited changes. These data have implications for the prospect of targeting miRNAs for CHC therapy.

[Abstract reproduced by permission of Nat Med 2009;15:31–33]

Abbreviations: CHC, chronic hepatitis C, cEVR, complete early virological responder, HCV, hepatitis C virus, HIV, human immunodeficiency virus, IFN, interferon, miRNAs, microRNAs, PKR, protein kinase R, PNR, primary nonresponder, RISC, RNA induced silencing complex, UTR, untranslated region

 

☆ The authors who have taken part in this study declared that they do not have anything to disclose regarding funding from industry or conflict of interest with respect to this manuscript.

PII: S0168-8278(09)00166-4

doi:10.1016/j.jhep.2009.03.018

Journal of Hepatology
Volume 51, Issue 3 , Pages 606-609, September 2009

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