Structural requirements for recognition of the human immunodeficiency virus type 1 core during host restriction in owl monkey cells
Structural requirements for recognition of the human immunodeficiency virus type 1 core during host restriction in owl monkey cells
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DOI：
10.1128/jvi.79.2.869-875.2005
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发表时间：
2005-01-01
影响因子：
5.4
通讯作者：
Aiken, C
中科院分区：
文献类型：
--
作者：
Forshey, BM;Shi, J;Aiken, C
人类免疫缺陷病毒1型（HIV-1）感染猴细胞在感染后早期受到宿主因素的限制，其作用机制尚不清楚。这些因子靶向病毒衣壳蛋白（CA）并减弱逆转录，表明它们与HIV-1核心结合并干扰其脱壳。为了鉴定衣壳中的相关结合决定簇，我们测试了在CA中含有Gag切割位点突变和氨基酸取代的病毒抑制猫头鹰猴细胞中野生型HIV-1报告病毒的限制的能力。结果表明，一个稳定的，聚合的衣壳和正确折叠的氨基末端CA亚基界面是必不可少的饱和宿主限制在靶细胞的HIV-1核心。我们的结论是，猫头鹰猴细胞限制性机械识别CA分子的聚合物阵列，最有可能通过直接参与的HIV-1衣壳在靶细胞前脱壳。
Human immunodeficiency virus type 1 (HIV-1) infection of simian cells is restricted at an early postentry step by host factors whose mechanism of action is unclear. These factors target the viral capsid protein (CA) and attenuate reverse transcription, suggesting that they bind to the HIV-1 core and interfere with its uncoating. To identify the relevant binding determinants in the capsid, we tested the capacity of viruses containing Gag cleavage site mutations and amino acid substitutions in CA to inhibit restriction of a wild type HIV-1 reporter virus in owl monkey cells. The results demonstrated that a stable, polymeric capsid and a correctly folded amino-terminal CA subunit interface are essential for saturation of host restriction in target cells by HIV-1 cores. We conclude that the owl monkey cellular restriction machinery recognizes a polymeric array of CA molecules, most likely via direct engagement of the HIV-1 capsid in target cells prior to uncoating.