Nishiyama Y, Ito Y, Shimokata K, Nagata I, Kurachi N, Sugiura Y
Microbiol Immunol. 1977;21(12):693-702. doi: 10.1111/j.1348-0421.1977.tb00338.x.
Infection of mouse L cells with vesicular stomatitis virus (VSV) leads to an extensive cell fusion, while porcine kidney stable (PS) cells infected with VSV show only cell rounding. Therefore, comparative morphological studies on the infection of the two cell lines were carried out using a transmission or scanning electron microscope and an immunofluorescence microscope. PS cells infected with VSV contrasted to L cells infected with the same virus in the following two points; (1) the principal site of VSV maturation was the intracytoplasmic vacuolar membrane in PS cells and the plasma membrane in L cells. However, it was found that viral glycoprotein was present on the cell surface of infected PS cells; (2) the morphological changes at the cell surface of infected PS cells occurred much earlier and were severer than those at the cell surface of infected L cells. From these observations, we discuss the possibility that the surfaceembrane of PS cells is too sensitive to the VSV-induced cell damage to cause cell fusion.
用水疱性口炎病毒(VSV)感染小鼠L细胞会导致广泛的细胞融合,而感染VSV的猪肾稳定(PS)细胞仅表现出细胞变圆。因此,使用透射或扫描电子显微镜以及免疫荧光显微镜对这两种细胞系的感染进行了比较形态学研究。感染VSV的PS细胞与感染相同病毒的L细胞在以下两点形成对比:(1)VSV成熟的主要部位在PS细胞的胞质内液泡膜和L细胞的质膜上。然而,发现病毒糖蛋白存在于感染的PS细胞的细胞表面;(2)感染的PS细胞表面的形态变化比感染的L细胞表面的形态变化发生得更早且更严重。基于这些观察结果,我们讨论了PS细胞的表面膜对VSV诱导的细胞损伤过于敏感以至于无法引起细胞融合的可能性。