Ion channel activity of HIV-1 Vpu is dispensable for counteraction of CD317
Ion channel activity of HIV-1 Vpu is dispensable for counteraction of CD317
复制标题
DOI：
10.1016/j.virol.2011.04.009
复制
发表时间：
2011-07-01
期刊：
影响因子：
3.7
通讯作者：
Schubert, Ulrich
中科院分区：
文献类型：
--
作者：
Bolduan, Sebastian;Votteler, Joerg;Schubert, Ulrich
虽然HIV-1 Vpu的C-末端结构域对于CD 4降解至关重要，但跨膜结构域（TM）介导离子通道活性，增强病毒释放，并且对于抵消CD 317/Bst-2/Tetherin至关重要。在这里，我们分析了是否需要Vpu的离子通道活性来拮抗CD 317介导的病毒体释放的限制。我们研究了三个保守残基的TM突变体：S23 A突变，这是以前被证明废除离子通道功能，不影响Vpu介导的病毒释放增强。相反，A14 N和A18 N突变不影响Vpu的离子通道活性，但显著降低了其支持病毒释放和下调细胞表面CD 317的能力。总之，我们的数据表明，不是Vpu的离子通道活性，但其从细胞表面去除CD 317的能力是增加HIV-1释放所必需的。(C)2011 Elsevier Inc. All rights reserved.
While the C-terminal domain of HIV-1 Vpu is critical for CD4 degradation, the transmembrane domain (TM) mediates ion channel activity, enhances virus release and is essential for counteracting CD317/Bst-2/Tetherin. Here we analyzed whether the ion channel activity of Vpu is required to antagonize CD317-mediated restriction of virion release. We examined TM-mutants of three conserved residues: the S23A mutation, which was previously shown to abrogate ion channel function, did not affect Vpu mediated augmentation of virus release. In contrast, the A14N and A18N mutation did not affect ion channel activity of Vpu, but substantially reduced its ability to support virus release and to down-regulate CD317 from the cell surface. Altogether, our data suggest that not the ion channel activity of Vpu, but its ability to remove CD317 from the cell surface is required to augment HIV-1 release. (C) 2011 Elsevier Inc. All rights reserved.