Pseudotyping human immunodeficiency virus type 1 by vesicular stomatitis virus G protein does not reduce the cell-dependent requirement of Vif for optimal infectivity: functional difference between Vif and Nef
Pseudotyping human immunodeficiency virus type 1 by vesicular stomatitis virus G protein does not reduce the cell-dependent requirement of Vif for optimal infectivity: functional difference between Vif and Nef
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DOI：
10.1099/0022-1317-80-11-2945
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发表时间：
1999-11-01
影响因子：
3.8
通讯作者：
Adachi, A
中科院分区：
文献类型：
--
作者：
Akari, H;Uchiyama, T;Adachi, A
Vif和Nef在人类免疫缺陷病毒1型（HIV-1）感染中的功能有一些相似之处：Vif和Nef依赖的HIV-1复制增强是细胞类型特异性的，这些基因的缺陷突变导致受感染细胞中前病毒DNA合成受限。最近已经表明，通过水泡性口炎病毒（VSV-G）的包膜糖蛋白对HIV-1进行假型化，靶向HIV-1进入内吞途径，并抑制病毒感染性对Nef的需求。在这项研究中，我们检查了VSV-G假型化是否抑制了Vif对HIV-1感染性的需求。结果发现，通过VSV-G假分型HIV-1并不能补偿Vif功能。连同Vif不影响Env的病毒结合/进入和病毒粒子掺入的发现，可以得出结论，Vif通过与Nef不同的机制独立于Env功能在进入后步骤增强HIV-1感染性。
The functions of Vif and Nef in human immunodeficiency virus type 1 (HIV-1) infection have some similarities: Vif- and Nef-dependent enhancement of HIV-1 replication is cell type-specific, and defective mutations in these genes result in restricted proviral DNA synthesis in infected cells. It has recently been shown that pseudotyping HIV-1 by the envelope glycoprotein of vesicular stomatitis virus (VSV-G) targets HIV-1 entry to an endocytic pathway and suppresses the requirement of Nef for virus infectivity. In this study, we examined whether VSV-G pseudotyping suppresses the requirement of Vif for HIV-1 infectivity. It was found that pseudotyping HIV-1 by VSV-G did not compensate for the Vif function. Together with the findings that Vif does not influence virus binding/entry and virion incorporation of Env, it is concluded that Vif enhances HIV-1 infectivity at the post-entry step(s) independently of the Env function by a different mechanism to that of Nef.