病毒蛋白Vpx诱导抗病毒因子SAMHD1蛋白酶体降解的研究进展

Jingwei Hou, Juan Du, Ke Zhao, Xiaofang Yu
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引用次数: 0

摘要

艾滋病毒是导致艾滋病传播的病原体,艾滋病与高死亡率有关。Vpx在HIV-2/SIV中表达,并在特定细胞中促进逆转录病毒感染。这种促进是通过vpx诱导的CRL4E3复合物的形成实现的,该复合物通过蛋白酶体降解去除内源性SAMHD1。SAMHD1的多个域(例如:(n端、核定位信号、连接子、HD结构域和c端)是vpx诱导降解的必要条件。不表达Vpx的hiv -1也进化出了绕过或抑制SAMHD1抗病毒功能的机制,例如对低水平dNTPs的耐受性和通过细胞周期蛋白L2诱导SAMHD1降解。基于以往的报告,以及该领域的最新发现,本文重点综述了vpx介导的SAMHD1降解机制及其促进hiv -1感染的机制。
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[Research Progress in Viral Protein Vpx induction of Proteasomal Degradation of the Antiviral Factor SAMHD1].

HIV the pathogen responsible for the transmission of AIDS, which is associated with a high mortality rate. Vpx is expressed in HIV-2/SIV and promotes retroviral infection in specific cells. This promotion is achieved by Vpx-induced formation of the CRL4E3 complex, which removes the endogenous SAMHD1 via proteasomal degradation. Multiple domains of SAMHD1(e.g., N-terminus, nuclear localization signal, linker, HD domain, and C-terminus)are essential for Vpx-induced degradation.HIV-1that does not express Vpx is also evolved with mechanisms to bypass or suppress the antiviral function of SAMHD1,such as the tolerance against a low level of dNTPs and induction of SAMHD1 degradation through cyclin L2.Based on previous reports published chronologically, as well as the latest findings in the field, this review focuses on the mechanism of Vpx-mediated degradation of SAMHD1,and its promotion of HIV-1infection.

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