APOBEC3-independent interferon-induced viral clearance in hepatitis B virus transgenic mice.

Abstract

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.

• Authors: Priscilla Turelli, Alexandra Liagre-Quazzola, Bastien Mangeat, Sonia Verp, Stephanie Jost, Didier Trono
• Journal: Journal of virology (J Virol) Vol. 82 Issue 13 Pg. 6585-90 (Jul 2008) ISSN: 1098-5514 [Electronic] United States
• PMID: 18434399 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• DNA Primers
• Interferons
• Apobec3 protein, mouse
• Cytidine Deaminase

Topics

• Animals
• Cytidine Deaminase (metabolism)
• DNA Primers (genetics)
• Gene Expression Regulation (drug effects)
• Genotype
• Hepatitis B (drug therapy, virology)
• Hepatitis B virus
• Immunoprecipitation
• Interferons (pharmacology, therapeutic use)
• Mice
• Mice, Transgenic
• Reverse Transcriptase Polymerase Chain Reaction
• Virus Replication (drug effects, genetics)