TRIM5α and Species Tropism of HIV/SIV.
TRIM5α and Species Tropism of HIV/SIV.
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DOI：
10.3389/fmicb.2012.00013
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发表时间：
2012
影响因子：
5.2
通讯作者：
Shioda T
中科院分区：
文献类型：
--
作者：
Nakayama EE;Shioda T
人类免疫缺陷病毒1型（HIV-1）感染人类和黑猩猩，但不感染旧世界猴（OWM），如恒河猴（Rh）和食蟹猴（CM）。HIV-1有效地进入OWM细胞，但在逆转录前遇到阻滞。这种狭窄的宿主范围归因于宿主细胞中的屏障。2004年，通过对Rh cDNA文库的筛选，确定了三重基序5α（TRIM 5 α）为细胞抗病毒因子。TRIM 5 α是TRIM 5基因产生的剪接变体之一，TRIM 5蛋白是TRIM家族的成员，包含RING、B-box 2和卷曲螺旋结构域。RING结构域经常在E3泛素连接酶中发现，TRIM 5 α通过泛素-蛋白酶体依赖性途径降解。在TRIM 5剪接变体中，TRIM 5 α单独具有额外的C末端PRYSPRY（B30.2）结构域。先前的研究表明，不同猴种之间PRYSPRY结构域可变区的序列变异会影响种特异性逆转录病毒感染，而病毒衣壳蛋白的氨基酸序列差异决定了病毒对限制性内切酶的敏感性。TRIM 5 α通过其PRYSPRY结构域识别传入病毒的多聚化衣壳蛋白（病毒核心），因此被认为控制逆转录病毒感染。Rh-TRIM 5基因存在显著的种内变异。还报道了一些Rh和CM个体在TRIM 5基因中具有反转座亲环素A开放阅读框，其产生TRIM 5-亲环素A融合蛋白（TRIMCyp）。TRIMCyp最初被鉴定为新世界猫头鹰猴的抗HIV-1因子，是通过反转录转座获得新功能的有趣例子。由于Rh的不同TRIM 5基因型在体内表现出不同水平的猴免疫缺陷病毒复制，因此认为TRIM 5基因分型在获得性免疫缺陷综合征猴模型中是重要的。
Human immunodeficiency virus type 1 (HIV-1) infects humans and chimpanzees but not old world monkeys (OWMs) such as the rhesus monkey (Rh) and cynomolgus monkey (CM). HIV-1 efficiently enters cells of OWMs but encounters a block before reverse transcription. This narrow host range is attributed to a barrier in the host cell. In 2004, the screening of a Rh cDNA library identified tripartite motif 5α (TRIM5α) as a cellular antiviral factor. TRIM5α is one of splicing variants produced by TRIM5 gene and TRIM5 proteins are members of the TRIM family containing RING, B-box 2, and coiled-coil domains. The RING domain is frequently found in E3 ubiquitin ligase and TRIM5α is degraded via the ubiquitin–proteasome-dependent pathway. Among TRIM5 splicing variants, TRIM5α alone has an additional C-terminal PRYSPRY (B30.2) domain. Previous studies have shown that sequence variation in variable regions of the PRYSPRY domain among different monkey species affects species-specific retrovirus infection, while amino acid sequence differences in the viral capsid protein determine viral sensitivity to restriction. TRIM5α recognizes the multimerized capsid proteins (viral core) of an incoming virus by its PRYSPRY domain and is thus believed to control retroviral infection. There are significant intraspecies variations in the Rh-TRIM5 gene. It has also been reported that some Rh and CM individuals have retrotransposed cyclophilin A open reading frame in the TRIM5 gene, which produces TRIM5–cyclophilin A fusion protein (TRIMCyp). TRIMCyp, which was originally identified as an anti-HIV-1 factor of New World owl monkeys, is an interesting example of the gain of a new function by retrotransposition. As different TRIM5 genotypes of Rh showed different levels of simian immunodeficiency virus replication in vivo, the TRIM5 genotyping is thought to be important in acquired immunodeficiency syndrome monkey models.
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