Nomaguchi Masako, Doi Naoya, Matsumoto Yui, Sakai Yosuke, Fujiwara Sachi, Adachi Akio
Department of Microbiology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
Front Microbiol. 2012 Jul 26;3:267. doi: 10.3389/fmicb.2012.00267. eCollection 2012.
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.
1型人类免疫缺陷病毒（HIV-1）仅对人类具有嗜性和致病性，在常用于实验感染的猕猴中不复制。这种特别狭窄的宿主范围（物种嗜性）极大地阻碍了HIV-1/获得性免疫缺陷综合征（AIDS）基础研究的进展。对其潜在机制的广泛研究表明，病毒辅助蛋白之一的Vif除了对Gag衣壳蛋白外，对HIV-1的物种嗜性也至关重要。另一种辅助蛋白Vpu也已被证明会影响HIV-1的这一特性。在本综述中，我们重点关注这些HIV-1蛋白与物种特异性限制因子的功能相互作用。此外，我们描述了一种与由辅助蛋白控制的HIV-1物种嗜性相关的进化观点。
