Species tropism of HIV-1 modulated by viral accessory proteins

被引:5
|
作者
Nomaguchi, Masako [1 ]
Doi, Naoya [1 ]
Matsumoto, Yui [1 ]
Sakai, Yosuke [1 ]
Fujiwara, Sachi [1 ]
Adachi, Akio [1 ]
机构
[1] Univ Tokushima, Grad Sch, Inst Hlth Biosci, Dept Microbiol, Tokushima 7708503, Japan
关键词
HIV-1; species tropism; accessory protein; Vif; Vpu;
D O I
10.3389/fmicb.2012.00267
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Human immunodeficiency virus type 1 (HIV-1) is tropic and pathogenic only for humans, and does not replicate in macaque monkeys routinely used for experimental infections. This specially narrow host range (species tropism) has impeded much the progress of HIV-1/acquired immunodeficiency syndrome (AIDS) basic research. Extensive studies on the underlying mechanism have revealed that Vif, one of viral accessory proteins, is critical for the HIV-1 species tropism in addition to Gag-capsid protein. Another auxiliary protein Vpu also has been demonstrated to affect this HIV-1 property. In this review, we focus on functional interactions of these HIV-1 proteins and species specific-restriction factors. In addition, we describe an evolutional viewpoint that is relevant to the species tropism of HIV-1 controlled by the accessory proteins.
引用
收藏
页数:6
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