Tetherin antagonism by primate lentiviral nef proteins.
Tetherin antagonism by primate lentiviral nef proteins.
复制标题
灵长类慢病毒 nef 蛋白的 Tetherin 拮抗作用。
DOI：
10.2174/157016211798842044
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发表时间：
2011
影响因子：
1
通讯作者：
F. Kirchhoff
中科院分区：
文献类型：
--
作者：
D. Sauter;F. Kirchhoff
灵长类慢病毒的多功能Nef蛋白通常被认为是一种早期病毒因子，它从细胞表面下调各种受体并调节几种信号通路，以促进病毒免疫逃避并使细胞有利于病毒复制。然而，Nef也在感染的后期阶段起作用，例如通过增加子代病毒粒子的传染性。就在最近，人们已经清楚地发现，在大约40种不同的猴子和类人猿物种中检测到的许多灵长类慢病毒也使用Nef来拮抗拴链蛋白（BST2/CD317），拴链蛋白是一种通过将新生病毒颗粒拴在细胞表面来抑制病毒释放的细胞因子。例外情况是一些感染尾猿猴的猿类免疫缺陷病毒（siv），它们使用其附属Vpu蛋白来抵消拴链蛋白的限制。此外，大流行HIV-1 M组毒株在分别从黑猩猩和黑白鹭的人畜共患传播后，从Nef转变为Vpu， HIV-2 A组毒株从Nef转变为Env，以对抗人类的tetherin限制。这些进化开关很可能是由人类系链蛋白同源物细胞质域的缺失造成的，该区域赋予了对Nef的抗性。在这里，我们总结了目前关于nef介导的tetherin拮抗的一些知识。
The multifunctional Nef protein of primate lentiviruses is commonly considered an early viral factor that down-modulates various receptors from the cell surface and modulates several signaling pathways to facilitate viral immune evasion and to render the cell conducive for viral replication. However, Nef also acts during the late stages of infection, e.g. by increasing the infectivity of progeny virions. Just recently, it has become clear that many primate lentiviruses that have been detected in about 40 different monkey and ape species also use Nef to antagonize tetherin (BST2/CD317), a cellular factor that inhibits virus release by tethering nascent viral particles to the cell surface. Exceptions are some simian immunodeficiency viruses (SIVs) infecting Cercopithecus monkeys that employ their accessory Vpu protein to counteract the restriction by tetherin. Furthermore, pandemic HIV-1 group M strains switched from Nef to Vpu and HIV-2 group A isolates from Nef to Env after zoonotic transmission from chimpanzees and sooty mangabeys, respectively, to antagonize the tetherin restriction in humans. These evolutionary switches were most likely enforced by a deletion in the cytoplasmic domain of the human tetherin orthologue that confers resistance to Nef. Here, we summarize some of our current knowledge about Nef-mediated tetherin antagonism.