MECHANISM OF POLYKARYOCYTE INDUCTION BY VESICULAR STOMATITIS-VIRUS IN RAT XC-CELLS
MECHANISM OF POLYKARYOCYTE INDUCTION BY VESICULAR STOMATITIS-VIRUS IN RAT XC-CELLS
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DOI：
10.1099/0022-1317-34-2-305
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发表时间：
1977-01-01
影响因子：
3.8
通讯作者：
LAFAY, F
中科院分区：
文献类型：
--
作者：
CHANYFOURNIER, F;CHANY, C;LAFAY, F
水疱性口炎病毒 (VSV) 在劳斯肉瘤病毒布拉格株（XC 细胞）转化的大鼠胚胎成纤维细胞中诱导多核细胞。细胞融合需要细胞中病毒的脱壳、正常结构的 G 和 M 蛋白的合成以及它们并入细胞膜。完全感染性病毒的合成是不必要的。除了这些抗原之外，宿主膜的特殊但未定义的构成也很重要。对于 G 和 M 抗原无缺陷的热敏突变体，细胞融合在非允许温度 (39.6°C) 下比在允许温度 (31°C) 下广泛得多。使用利福平敏感突变体也显示了这 2 种抗原的重要性。这两种抗原可能会在细胞膜中诱导磷脂分布不平衡，然后磷脂通过膜连接处扩散到周围细胞，从而引发细胞融合。
Vesicular stomatitis virus (VSV) induced 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.degree. C) than at the permissive one (31.degree. C). The importance of the 2 antigens is also shown using rifampicin-sensitive mutants. These 2 antigens may 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.