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Volume 15, No 11, Nov 2005

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 15 Issue 11, November 2005: 923-934

COMMENTARY

Roles of HIV-1 auxiliary proteins in viral pathogenesis and host-pathogen interactions

Lin LI1,5, Hai Shan LI3,6, C David PAUZA1,2,3, Michael BUKRINSKY4 and Richard Y ZHAO1,2,3

1Department of Pathology, University of Maryland, Baltimore, MD 21201, USA
2Department of Microbiology-Immunology, University of Maryland, Baltimore, MD 21201, USA
3Institute of Human Virology, University of Maryland, Baltimore, MD 21201, USA
4Department of Microbiology, Immunology and Tropic Medicine, George Washington University, Washington, DC 20037, USA
5AIDS Research Department, Beijing Institute of Microbiology and Epidemiology, Bejing 100071, China
6National Center for AIDS, China Centers for Disease Control, Beijing 100050, China
Correspondence: Richard Y ZHAO(rzhao@som.umaryland.edu)

Active host-pathogen interactions take place during infection of human immunodeficiency virus type 1 (HIV-1). Outcomes of these interactions determine the efficiency of viral infection and subsequent disease progression. HIV-infected cells respond to viral invasion with various defensive strategies such as innate, cellular and humoral immune antiviral mechanisms. On the other hand, the virus has also developed various offensive tactics to suppress these host cellular responses. Among many of the viral offensive strategies, HIV-1 viral auxiliary proteins (Tat, Rev, Nef, Vif, Vpr and Vpu) play important roles in the host-pathogen interaction and thus have significant impacts on the outcome of HIV infection. One of the best examples is the interaction of Vif with a host cytidine deaminase APOBEC3G. Although specific roles of other auxiliary proteins are not as well described as Vif-APOBEC3G interaction, it is the goal of this brief review to summarize some of the preliminary findings with the hope to stimulate further discussion and investigation in this exhilarating area of research


Cell Research (2005) 15, 923–934. doi:10.1038/sj.cr.7290370

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