Riedel H, Kondor-Koch C, Garoff H
EMBO J. 1984 Jul;3(7):1477-83. doi: 10.1002/j.1460-2075.1984.tb01999.x.
Vesicular stomatitis virus (VSV) enters the host cell by the receptor-mediated endocytotic pathway. This brings the virus particle into acidic vesicles inside the cell where infection occurs through a fusion event between the viral and the host vesicle membrane. In this work we have shown that the VSV glycoprotein (G) carries the fusion activity of this virus. The G protein was expressed on the surface of baby hamster kidney 21 cells from cloned cDNA which had been engineered into an expression vector and introduced into cell nuclei with the aid of a glass microneedle. A short (60 s) treatment with acid (pH less than or equal to 6.0) medium induced fusion of cells having G protein on their surface. For efficient G protein expression and cell-cell fusion we had to trim the 5' end of the G cDNA and to use as promoter the long terminal repeat of the mouse Moloney sarcoma virus.
水泡性口炎病毒（VSV）通过受体介导的内吞途径进入宿主细胞。这将病毒颗粒带入细胞内的酸性囊泡中，在那里通过病毒与宿主囊泡膜之间的融合事件发生感染。在这项工作中，我们已经表明VSV糖蛋白（G）具有该病毒的融合活性。G蛋白从克隆的cDNA在婴儿仓鼠肾21细胞表面表达，该cDNA已被构建到表达载体中，并借助玻璃微针引入细胞核。用酸性（pH小于或等于6.0）培养基进行短时间（60秒）处理可诱导表面带有G蛋白的细胞融合。为了实现高效的G蛋白表达和细胞间融合，我们必须修剪G cDNA的5'末端，并使用小鼠莫洛尼肉瘤病毒的长末端重复序列作为启动子。
