Influence of gag on human immunodeficiency virus type 1 species-specific tropism
Influence of gag on human immunodeficiency virus type 1 species-specific tropism
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DOI：
10.1128/jvi.78.21.11816-11822.2004
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发表时间：
2004-11-01
影响因子：
5.4
通讯作者：
Towers, GJ
中科院分区：
文献类型：
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作者：
Ikeda, Y;Ylinen, LMJ;Towers, GJ
人类免疫缺陷病毒1型（HIV-1）的宿主范围较窄，部分原因是人类（Ref 1）和猴（Lv 1）中的主要作用限制因子。在这里，我们表明，gag编码种特异性慢病毒感染的决定因素，部分相关的限制因素。衣壳和宿主亲环素A（CypA）之间的相互作用可以保护HIV-1在人类细胞中免受限制，但对于猿猴细胞中的最大限制是必不可少的。我们发现，HIV-1分离株之间的序列变异导致人类和猿细胞对限制性因子的敏感性发生变化。我们提出了进一步的证据的重要性，靶细胞CypA的CypA包装在病毒体中，特别是在gp 160假型HIV-1载体的背景下。我们还表明，限制的敏感性是由H87 Q突变的衣壳，牵连在HIV-1的免疫控制，可能连接免疫和先天控制HIV-1感染。
The narrow host range of human immunodeficiency virus type 1 (HIV-1) is due in part to dominant acting restriction factors in humans (Ref1) and monkeys (Lv1). Here we show that gag encodes determinants of species-specific lentiviral infection, related in part to such restriction factors. Interaction between capsid and host cyclophilin A (CypA) protects HIV-1 from restriction in human cells but is essential for maximal restriction in simian cells. We show that sequence variation between HIV-1 isolates leads to variation in sensitivity to restriction factors in human and simian cells. We present further evidence for the importance of target cell CypA over CypA packaged in virions, specifically in the context of gp160 pseudotyped HIV-1 vectors. We also show that sensitivity to restriction is controlled by an H87Q mutation in the capsid, implicated in the immune control of HIV-1, possibly linking immune and innate control of HIV-1 infection.