Retained in vitro infectivity and cytopathogenicity of HIV-1 despite truncation of the C-terminal tail of the env gene product.
Retained in vitro infectivity and cytopathogenicity of HIV-1 despite truncation of the C-terminal tail of the env gene product.
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尽管 env 基因产物的 C 末端尾部被截断，但仍保留了 HIV-1 的体外感染性和细胞致病性。
DOI：
10.1016/0042-6822(92)90692-i
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发表时间：
1992
期刊：
影响因子：
3.7
通讯作者：
V. Bosch
中科院分区：
文献类型：
--
作者：
T. Wilk;T. Pfeiffer;V. Bosch
在HIV-1的env基因中产生了5个帧内停止突变，这些突变导致env基因产物在细胞质c端尾部被截断，并分析了它们对膜融合能力、糖蛋白融入病毒颗粒、传染性和细胞致病性的影响。由此产生的截断的糖蛋白被正常加工，被运输到细胞表面，并能够诱导cd4依赖的膜融合。其中一个被截断144个氨基酸的突变糖蛋白的膜融合能力提高到野生型糖蛋白的两倍左右。除了一个例外，截断的病毒糖蛋白被整合到病毒颗粒中，这对允许的MT-4细胞具有传染性和细胞病变性。然而，与野生型病毒感染相比，突变病毒的感染动力学有不同程度的延迟。然而，在每种情况下，在受感染的培养物中，PCR扩增和病毒DNA的直接测序证实了突变体的存在和反向DNA的缺失。突变病毒编码一个截断最长的病毒糖蛋白（144个氨基酸），其中gp41仅保留7个细胞质c端氨基酸，导致MT-4细胞的感染动力学与野生型病毒相比仅略微延迟。这意味着gp41的c端144个氨基酸不是糖蛋白整合到病毒颗粒中所必需的，也不会显著促进MT-4细胞中HIV-1的感染性和细胞致病性。
Five in-frame stop mutations in the HIV-1 env gene, which lead to the production of env gene products truncated within the cytoplasmic C-terminal tail, have been generated and their effects on membrane fusion capacity, glycoprotein incorporation into virus particles, infectivity, and cytopathogenicity were analyzed. The resulting truncated glycoproteins were processed normally, were transported to the cell surface, and were able to induce CD4-dependent membrane fusion. The membrane fusion capacity of one of the mutant glycoproteins with a truncation of 144 amino acids was increased to about double of that induced by wild-type glycoprotein. With a single exception, the truncated viral glycoproteins were incorporated into virus particles which were infectious and cytopathic for permissive MT-4 cells. The infection kinetics with the mutated viruses were, however, delayed to varying degrees in comparison to infection with wild-type virus. Nevertheless, in each case, PCR amplification and direct sequencing of viral DNA in the infected cultures confirmed the presence of the mutant and the absence of revertant DNA. The mutant virus encoding a viral glycoprotein with the longest truncation (144 amino acids), in which only 7 cytoplasmic C-terminal amino acids in gp41 remain, resulted in infection kinetics in MT-4 cells which were only marginally delayed in comparison to those induced by wild-type virus. This means that these C-terminal 144 amino acids of gp41 are not necessary for glycoprotein incorporation into virus particles nor do they significantly contribute to the infectivity nor the cytopathogenicity of HIV-1 in MT-4 cells.
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影响因子：
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影响因子：
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作者：
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DOI：
10.1073/pnas.86.5.1495
发表时间：
1989-03-01
影响因子：
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作者：
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通讯作者：
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