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J Gen Virol 89 (2008), 722-730; DOI 10.1099/vir.0.83530-0

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APOBEC3G upregulation by alpha interferon restricts human immunodeficiency virus type 1 infection in human peripheral plasmacytoid dendritic cells

Feng-xiang Wang1, Jialing Huang1, Hangxiang Zhang2, Xinliang Ma2 and Hui Zhang1

1 Center for Human Virology, Division of Infectious Diseases, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
2 Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA

Correspondence
Hui Zhang
hui.zhang{at}jefferson.edu

APOBEC3G (A3G), a member of cytidine deaminase family, has potent anti-human immunodeficiency virus type 1 (HIV-1) activity. It has been demonstrated that alpha interferon (IFN-{alpha}) can significantly enhance the expression of A3G in human primary resting CD4+ T-cells, macrophages and primary hepatocytes, subsequently decreasing their viral susceptibility. Plasmacytoid dendritic cells (pDCs) are key effectors in innate host immunity, mediating adaptive immune responses and stimulating IFN-{alpha} production in reaction to various stimuli. In this report, we demonstrate that IFN-{alpha}, either exogenously added to- or endogenously secreted by pDCs, can enhance the expression of A3G and its family members such as A3A, A3C and A3F. We have also shown that IFN-{alpha} can inhibit HIV-1 expression in pDCs. This inhibitory effect could be countered by addition of an A3G-specific short interfering RNA, indicating that IFN-{alpha}-induced A3G plays a key role in mediating pDCs response to HIV-1. Given the central role played by pDCs in orchestrating the IFN-{alpha}/A3G intercellular network and intracellular signal pathway, our data indicate that pDCs themselves are also protected by an IFN-{alpha}/A3G-mediated innate immunity barrier from HIV-1 infection.




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