The human TRIM5α restriction factor mediates accelerated uncoating of the N-tropic murine leukemia virus capsid
The human TRIM5α restriction factor mediates accelerated uncoating of the N-tropic murine leukemia virus capsid
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DOI：
10.1128/jvi.02318-06
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发表时间：
2007-03-01
影响因子：
5.4
通讯作者：
Sodroski, Joseph
中科院分区：
文献类型：
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作者：
Perron, Michel J.;Stremlau, Matthew;Sodroski, Joseph
宿主细胞因子TRIM5 α（hu）和Fv-1分别在逆转录之前或之后的早期试验后步骤限制N-嗜性鼠白血病病毒（N-MLV）感染。有趣的是，MLV衣壳的残基110的身份决定了对TRIM5 α（hu）和Fv-1的易感性。在这项研究中，我们调查的命运MLV衣壳细胞表达TRIM5 α（人）或Fv-1限制性因子。TRIM5 α（hu）而非Fv-1的表达特异性地促进了感染细胞内颗粒N-MLV衣壳向可溶性衣壳蛋白的过早转化。TRIM5 α（hu）介导的颗粒N-MLV衣壳解体依赖于病毒衣壳的残基110。此外，TRIM5 α（hu）的缺失或破坏。有效的N-MLV限制所必需的结构域完全消除了用野生型TRIM 5 α（hu）观察到的颗粒状N-MLV衣壳的消失。这些结果表明，病毒衣壳的过早分解有助于TRIM alpha（hu）限制N-MLV感染，而不是Fv-1。
The host cell factors TRIM5 alpha(hu) and Fv-1 restrict N-tropic murine leukemia virus (N-MLV) infection at an early postentry step before or after reverse transcription, respectively. Interestingly, the identity of residue 110 of the MLV capsid determines susceptibility to both TRIM5 alpha(hu) and Fv-1. In this study, we investigate the fate of the MLV capsid in cells expressing either the TRIM5 alpha(hu) or Fv-1 restriction factor. The expression of TRIM5 alpha(hu), but not Fv-1, specifically promoted the premature conversion of particulate N-MLV capsids within infected cells to soluble capsid proteins. The TRIM5 alpha(hu)-mediated disassembly of particulate N-MLV capsids was dependent upon residue 110 of the viral capsid. Furthermore, the deletion or disruption of TRIM5 alpha(hu). domains necessary for potent N-MLV restriction completely abrogated the disappearance of particulate N-MLV capsids observed with wild-type TRIM5 alpha(hu). These results suggest that premature disassembly of the viral capsid contributes to the restriction of N-MLV infection by TRIM alpha(hu), but not by Fv-1.