Functional interactions between herpes simplex virus pUL51, pUL7 and gE reveal cell-specific mechanisms for epithelial cell-to-cell spread
Functional interactions between herpes simplex virus pUL51, pUL7 and gE reveal cell-specific mechanisms for epithelial cell-to-cell spread
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DOI：
10.1016/j.virol.2019.08.014
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发表时间：
2019-11-01
期刊：
影响因子：
3.7
通讯作者：
Roller, Richard J.
中科院分区：
文献类型：
--
作者：
Feutz, Erika;McLeland-Wieser, Hilary;Roller, Richard J.
单纯疱疹病毒在上皮细胞间的传播是由病毒被膜和包膜蛋白复合物介导的，包括gE/gI和pUL51/pUL7。在感染细胞中，pUL51与pUL7和gE/gI相互作用。我们发现，pUL51的氨基酸30-90介导了与pUL7的相互作用。我们还发现，pUL51的167-244氨基酸缺失或pUL7表达减少都会导致gE无法集中在Vero细胞的连接表面。我们还通过分析gE/UL51双突变体的表型，验证了gE和pUL51在细胞间传播的相同途径上起作用的假设。在HaCaT细胞中，pUL51和gE在相同的扩散途径上起作用，而在Vero细胞中，它们在不同的途径上起作用。gE基因的缺失强烈增强了病毒在Vero细胞中向培养基中的释放，这表明依赖gE的传播途径可能与视觉向培养基中的释放竞争。
Herpes simplex virus spread between epithelial cells is mediated by virus tegument and envelope protein complexes including gE/gI and pUL51/pUL7. pUL51 interacts with both pUL7 and gE/gI in infected cells. We show that amino acids 30-90 of pUL51 mediate interaction with pUL7. We also show that deletion of amino acids 167-244 of pUL51, or ablation of pUL7 expression both result in failure of gE to concentrate at junctional surfaces of Vero cells. We also tested the hypothesis that gE and pUL51 function on the same pathway for cell-tocell spread by analyzing the phenotype of a double gE/UL51 mutant. In HaCaT cells, pUL51 and gE function on the same spread pathway, whereas in Vero cells they function on different pathways. Deletion of the gE gene strongly enhanced virus release to the medium in Vero cells, suggesting that the gE-dependent spread pathway may compete with vision release to the medium.