Characterization of cell-cell fusion mediated by herpes simplex virus 2 glycoproteins gB, gD, gH and gL in transfected cells
Characterization of cell-cell fusion mediated by herpes simplex virus 2 glycoproteins gB, gD, gH and gL in transfected cells
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DOI：
10.1099/0022-1317-81-8-2017
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发表时间：
2000-08-01
影响因子：
3.8
通讯作者：
Muggeridge, MI
中科院分区：
文献类型：
--
作者：
Muggeridge, MI
单纯疱疹病毒（HSV）在进入细胞时介导其包膜和质膜之间的融合，以及在邻近感染细胞和未感染细胞的质膜之间形成多核巨细胞的机制尚不清楚。病毒-细胞融合需要四种病毒糖蛋白（gB, gD， gH和gL），而细胞-细胞融合（合胞体形成）需要这些加上其他几种病毒糖蛋白。一个模型系统的可用性将有助于更好的理解，在没有感染的情况下，可以用最少的一组蛋白质诱导融合。目前已经开发出一种适用于HSV-2的系统，使用转染的COS7、293或HEp-2细胞。在这种系统中，引起细胞-细胞融合所需的HSV-2蛋白的最小集合是gB、gD、gH和gL，它看起来类似于病毒-细胞融合，而不是合胞体的形成。然而，gB中的一个突变能够增强转染细胞和感染细胞的融合，而对病毒与细胞的融合没有影响，这表明了相反的结论。一组抗hsv抗体和融合抑制剂环孢素a的不同作用证实，转染细胞的融合与病毒-细胞融合和合胞体形成有一些共同的特性。因此，它可能有助于确定这些过程的不同之处，并有助于检验这样一种假设，即一些病毒蛋白会阻止膜融合，直到病毒生命周期的适当点，然后其他蛋白质会克服这一障碍。
The mechanisms by which herpes simplex viruses (HSV) mediate fusion between their envelope and the plasma membrane during entry into cells, and between the plasma membranes of adjacent infected and uninfected cells to form multinucleated giant cells, are poorly understood, Four viral glycoproteins (gB, gD, gH and gL) are required for virus-cell fusion, whereas these plus several others are required for cell-cell fusion (syncytium formation). A better understanding would be aided by the availability of a model system, whereby fusion could be induced with a minimal set of proteins, in the absence of infection. A suitable system has now been developed for HSV-2, using transfected COS7, 293 or HEp-2 cells, Insofar as the minimal set of HSV-2 proteins required to cause cell-cell fusion in this system is gB, gD, gH and gL, it would appear to resemble virus-cell fusion rather than syncytium formation. However, the ability of a mutation in gB to enhance the fusion of both transfected cells and infected cells, while having no effect on virus-cell fusion, points to the opposite conclusion. The differential effects of a panel of anti-HSV antibodies, and of the fusion-inhibitor cyclosporin A, confirm that the fusion of transfected cells shares some properties with virus-cell fusion and others with syncytium formation. It may therefore prove useful for determining how these processes differ, and for testing the hypothesis that some viral proteins prevent membrane fusion until the appropriate point in the virus life-cycle, with other proteins then overcoming this block.