%0 Journal Article %A Wang, Feng-xiang %A Huang, Jialing %A Zhang, Hangxiang %A Ma, Xinliang %A Zhang, Hui %T APOBEC3G upregulation by alpha interferon restricts human immunodeficiency virus type 1 infection in human peripheral plasmacytoid dendritic cells %D 2008 %J Journal of General Virology, %V 89 %N 3 %P 722-730 %@ 1465-2099 %R https://doi.org/10.1099/vir.0.83530-0 %I Microbiology Society, %X 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-α) 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-α production in reaction to various stimuli. In this report, we demonstrate that IFN-α, 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-α 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-α-induced A3G plays a key role in mediating pDCs response to HIV-1. Given the central role played by pDCs in orchestrating the IFN-α/A3G intercellular network and intracellular signal pathway, our data indicate that pDCs themselves are also protected by an IFN-α/A3G-mediated innate immunity barrier from HIV-1 infection. %U https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.83530-0