Roles of Virion-Incorporated CD162 (PSGL-1), CD43, and CD44 in HIV-1 Infection of T Cells.

Roles of Virion-Incorporated CD162 (PSGL-1), CD43, and CD44 in HIV-1 Infection of T Cells.
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病毒体结合的CD 162(PSGL-1)、CD 43和CD 44在HIV-1感染T细胞中的作用

DOI:
10.3390/v13101935
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发表时间:
2021-09-26
期刊:
Viruses
影响因子:
--
通讯作者:
Ono A
Ono A
中科院分区:
其他
文献类型:
--
作者:
Murakami T;Ono A

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新生的HIV-1颗粒在质膜组装过程中融合了病毒包膜糖蛋白和多个宿主跨膜蛋白。至少有一些位于病毒粒子表面的宿主跨膜蛋白被报道为亲病毒因子,它们通过与非T细胞的相互作用增强病毒与靶细胞的黏附或促进CD4+T细胞的反式感染。除了亲病毒因子,抗病毒跨膜蛋白还被掺入子代病毒粒子中。这些结合了病毒粒子的跨膜蛋白抑制了HIV-1在附着和融合时的进入。在被感染的极化的CD4+T细胞中,HIV-1 Gag定位于一个后端突起,称为尾足。无论细胞极化如何,Gag与尾足类定向宿主跨膜蛋白的一部分共定位并促进病毒粒子的掺入,包括CD162、CD43和CD44。直到最近,这些结合了病毒粒子的蛋白质的功能还不清楚。在这里,我们回顾了最近关于病毒粒子结合的CD162、CD43和CD44在HIV-1传播到CD4+T细胞中所起的作用的研究结果。
Nascent HIV-1 particles incorporate the viral envelope glycoprotein and multiple host transmembrane proteins during assembly at the plasma membrane. At least some of these host transmembrane proteins on the surface of virions are reported as pro-viral factors that enhance virus attachment to target cells or facilitate trans-infection of CD4+ T cells via interactions with non-T cells. In addition to the pro-viral factors, anti-viral transmembrane proteins are incorporated into progeny virions. These virion-incorporated transmembrane proteins inhibit HIV-1 entry at the point of attachment and fusion. In infected polarized CD4+ T cells, HIV-1 Gag localizes to a rear-end protrusion known as the uropod. Regardless of cell polarization, Gag colocalizes with and promotes the virion incorporation of a subset of uropod-directed host transmembrane proteins, including CD162, CD43, and CD44. Until recently, the functions of these virion-incorporated proteins had not been clear. Here, we review the recent findings about the roles played by virion-incorporated CD162, CD43, and CD44 in HIV-1 spread to CD4+ T cells.
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