Dienes H P, Knoblich A, Falke D
Arch Virol. 1985;86(3-4):223-37. doi: 10.1007/BF01309827.
Fibronectin is lost from the surface of HSV infected cells during cell rounding. In order to investigate also the fate of fibronectin during the process of HSV-induced cell-fusion, BHK, Vero as well as primary or secondary rabbit kidney cells were infected with HSV-1 strains producing cell-fusion. By immunofluorescence and immunoelectron microscopy a considerable loss of fibronectin after HSV infection could be demonstrated leaving only irregular clumps of fibronectin containing virus particles on the cell surface. Decrease and disarrangement of fibronectin was similar during cell rounding and cell fusion. Loss of Fibronectin was closely connected with the two types of the cytopathic effect (CPE) and could not be prevented by protease inhibitors. The immediate-early protein 175K is essential for induction of CPE and loss of fibronectin. The damage to the cell membrane during HSV infection shows certain analogous mechanisms with events induced by Cytochalasin B and might be explained by the loss of hypothetical fibronectin receptors.
在细胞变圆过程中,纤连蛋白从单纯疱疹病毒(HSV)感染的细胞表面丢失。为了研究在HSV诱导的细胞融合过程中纤连蛋白的命运,用产生细胞融合的HSV-1毒株感染了仓鼠肾细胞(BHK)、非洲绿猴肾细胞(Vero)以及原代或传代兔肾细胞。通过免疫荧光和免疫电子显微镜观察发现,HSV感染后纤连蛋白大量丢失,细胞表面仅留下含有病毒颗粒的不规则纤连蛋白团块。在细胞变圆和细胞融合过程中,纤连蛋白的减少和排列紊乱情况相似。纤连蛋白的丢失与两种细胞病变效应(CPE)密切相关,并且蛋白酶抑制剂无法阻止这种现象。即刻早期蛋白175K对于诱导CPE和纤连蛋白的丢失至关重要。HSV感染期间对细胞膜的损伤显示出与细胞松弛素B诱导的事件有某些类似机制,这可能是由于假定的纤连蛋白受体丢失所致。