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Journal of Virology, August 2006, p. 7645-7657, Vol. 80, No. 15
0022-538X/06/$08.00+0     doi:10.1128/JVI.00206-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Alpha Interferon Potently Enhances the Anti-Human Immunodeficiency Virus Type 1 Activity of APOBEC3G in Resting Primary CD4 T Cells

Keyang Chen, Jialing Huang, Chune Zhang, Sophia Huang, Giuseppe Nunnari, Feng-xiang Wang, Xiangrong Tong, Ling Gao, Kristi Nikisher, and Hui Zhang*

Center for Human Virology, Division of Infectious Diseases, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107

Received 27 January 2006/ Accepted 3 May 2006

The interferon (IFN) system, including various IFNs and IFN-inducible gene products, is well known for its potent innate immunity against wide-range viruses. Recently, a family of cytidine deaminases, functioning as another innate immunity against retroviral infection, has been identified. However, its regulation remains largely unknown. In this report, we demonstrate that through a regular IFN-{alpha}/ß signal transduction pathway, IFN-{alpha} can significantly enhance the expression of apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) in human primary resting but not activated CD4 T cells and the amounts of APOBEC3G associated with a low molecular mass. Interestingly, short-time treatments of newly infected resting CD4 T cells with IFN-{alpha} will significantly inactivate human immunodeficiency virus type 1 (HIV-1) at its early stage. This inhibition can be counteracted by APOBEC3G-specific short interfering RNA, indicating that IFN-{alpha}-induced APOBEC3G plays a key role in mediating this anti-HIV-1 process. Our data suggest that APOBEC3G is also a member of the IFN system, at least in resting CD4 T cells. Given that the IFN-{alpha}/APOBEC3G pathway has potent anti-HIV-1 capability in resting CD4 T cells, augmentation of this innate immunity barrier could prevent residual HIV-1 replication in its native reservoir in the post-highly active antiretroviral therapy era.

* Corresponding author. Mailing address: JAH334, 1040 Locust Street, Thomas Jefferson University, Philadelphia, PA 19107. Phone: (215) 503-0163. Fax: (215) 923-1956. E-mail: hui.zhang{at}jefferson.edu.

Journal of Virology, August 2006, p. 7645-7657, Vol. 80, No. 15
0022-538X/06/$08.00+0     doi:10.1128/JVI.00206-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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