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Journal of Virology, July 2008, p. 6585-6590, Vol. 82, No. 13
0022-538X/08/$08.00+0 doi:10.1128/JVI.00216-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Sonia Verp,
Stephanie Jost, and
Didier Trono*
Global Health Institute, School of Life Sciences and Frontiers in Genetics National Center for Competence in Research, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland
Received 30 January 2008/ Accepted 9 April 2008
Interferon (IFN) has been part of the standard treatment of chronic hepatitis B infection for more than 2 decades, yet the mechanism of action of this antiviral remains poorly understood. It was recently observed that members of the human APOBEC family of cytidine deaminases endowed with anti-hepatitis B virus (HBV) activity are upregulated by type I and II IFNs. However, we demonstrated that, in tissue culture, these cellular enzymes are not essential effectors of the anti-HBV action of these cytokines. Here, we show that murine APOBEC3 (muA3) can also block HBV replication. While expressed at low levels in the mouse liver at baseline, muA3 is upregulated upon IFN induction. However, in HBV-transgenic muA3 knockout mice, IFN induction blocked HBV DNA production as efficiently as in control HBV-transgenic muA3-competent animals. We conclude that APOBEC3 is not an essential mediator of the IFN-mediated inhibition of HBV in vivo.
Published ahead of print on 23 April 2008.
Present address: Departments of Dermatology and Venereology, Microbiology and Molecular Medicine, University Hospital and Medical School of Geneva, Geneva, Switzerland.
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