BST-2 介导的猴免疫缺陷病毒限制。
BST-2 mediated restriction of simian-human immunodeficiency virus.
机构信息
Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.
出版信息
Virology. 2010 Oct 25;406(2):312-21. doi: 10.1016/j.virol.2010.07.021. Epub 2010 Aug 13.
Abstract
Pathogenic simian-human immunodeficiency viruses (SHIV) contain HIV-1 Vpu and SIV Nef, both shown to counteract BST-2 (HM1.24; CD317; tetherin) inhibition of virus release in a species-specific manner. We show that human and pig-tailed BST-2 (ptBST-2) restrict SHIV. We found that sequential "humanization" of the transmembrane domain (TMD) of the pig-tailed BST-2 (ptBST-2) protein resulted in a fluctuation in sensitivity to HIV-1 Vpu. Our results also show that the length of the TMD in human and ptBST-2 proteins is important for BST-2 restriction and susceptibility to Vpu. Taken together, our results emphasize the importance of tertiary structure in BST-2 antagonism and suggests that the HIV-1 Vpu transmembrane domain may have additional functions in vivo unrelated to BST-2 antagonism.
摘要
致病性猴免疫缺陷病毒（SHIV）含有 HIV-1 Vpu 和 SIV Nef，两者均已被证明以种属特异性方式拮抗 BST-2（HM1.24；CD317； tetherin）对病毒释放的抑制作用。我们表明人类和猪尾 BST-2（ptBST-2）限制 SHIV。我们发现猪尾 BST-2（ptBST-2）蛋白跨膜域（TMD）的连续“人源化”导致对 HIV-1 Vpu 的敏感性波动。我们的结果还表明，人类和猪尾 BST-2 蛋白的 TMD 长度对于 BST-2 限制和对 Vpu 的易感性很重要。总之，我们的结果强调了 BST-2 拮抗作用中三级结构的重要性，并表明 HIV-1 Vpu 跨膜域在体内可能具有与 BST-2 拮抗无关的其他功能。
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