Chany-Fournier F, Chany C, Lafay F
J Gen Virol. 1977 Feb;34(2):305-14. doi: 10.1099/0022-1317-34-2-305.
Vesicular stomatitis virus (VSV) induces polykaryocytes in rat embryonic fibroblasts transformed by the Prague strain of Rous sarcoma virus (XC cells). The cell fusion requires the uncoating of the virus in the cell, the synthesis of normally structured G and M proteins and their incorporation into the cell membrane. The synthesis of fully infectious virus is unnecessary. In addition to these antigens, a special yet undefined constitution of the host membrane is also important. With thermosensitive mutants non-defective for G and M antigens, cell fusion is much more extensive at the non-permissive temperature (39-6 degrees C) than at the permissive one (31 degrees C). The importance of these two antigens is also shown using rifampicin-sensitive mutants. We postulate that these two antigens induce in the cell membrane an imbalance in the distribution of phospholipids which then diffuse through membrane junctions to surrounding cells, provoking thereafter the cell fusion.
水泡性口炎病毒（VSV）可在经劳氏肉瘤病毒布拉格株转化的大鼠胚胎成纤维细胞（XC细胞）中诱导多核细胞形成。细胞融合需要病毒在细胞内脱壳，合成正常结构的G蛋白和M蛋白并将它们整合到细胞膜中。合成完全有感染性的病毒并非必需。除了这些抗原外，宿主细胞膜的一种特殊但未明确的结构也很重要。对于G和M抗原无缺陷的温度敏感突变体，在非允许温度（39 - 6℃）下细胞融合比在允许温度（31℃）下更为广泛。使用对利福平敏感的突变体也表明了这两种抗原的重要性。我们推测这两种抗原在细胞膜中诱导磷脂分布失衡，然后磷脂通过膜连接扩散到周围细胞，从而引发细胞融合。
