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膜融合研究。IV. 海拉细胞与仙台病毒的融合

Studies of membrane fusion. IV. Fusion of HeLa cells with Sendai virus.

作者信息

Knutton S

出版信息

J Cell Sci. 1979 Apr;36:73-84. doi: 10.1242/jcs.36.1.73.

Abstract

The Sendai virus-induced fusion of HeLa cells has been studied by freeze-fracture electron microscopy. Freeze-fracture observations confirm previous scanning electron-microscope studies (1977) and show that at 4 degrees C virus particles bind to the cell surface and that cell agglutination results from the crosslinking by virus particles of microvilli on adjacent cells. Incubation at 37 degrees C initiates a change in viral envelope structure and fusion of 'altered' virus particles with the cell plasma membrane. Fusion of a virus particle with two crosslinked cells is probably the membrane fusion event which initiates cell-cell fusion; fusion is completed as a result of virally induced cell swelling. Lateral diffusion of viral envelope components following virus-cell fusion and, in some instances, an aggregation of plasma membrane intramembrane particles occurs in swollen cells. These observations show that the mechanisms of viral envelope-cell and probably cell-cell fusion are the same as have been reported for erythrocytes. Although endocytosis of intact virus particles does occur, the specialized cell-mediated mechanism for fusion of the viral envelope with the cell plasma membrane suggests that this, and not viropexis, is the mechanism of Sendai virus infection.

摘要

利用冷冻断裂电子显微镜对仙台病毒诱导的HeLa细胞融合进行了研究。冷冻断裂观察结果证实了先前扫描电子显微镜研究(1977年)的结果,并表明在4℃时病毒颗粒结合到细胞表面,且细胞凝集是由病毒颗粒使相邻细胞上的微绒毛交联所致。在37℃孵育会引发病毒包膜结构的变化以及“改变的”病毒颗粒与细胞质膜的融合。病毒颗粒与两个交联细胞的融合可能是引发细胞间融合的膜融合事件;由于病毒诱导的细胞肿胀,融合得以完成。病毒 - 细胞融合后病毒包膜成分的侧向扩散,以及在某些情况下肿胀细胞中质膜内膜颗粒的聚集也会发生。这些观察结果表明,病毒包膜 - 细胞以及可能的细胞 - 细胞融合机制与红细胞中所报道的机制相同。虽然完整病毒颗粒确实会发生内吞作用,但病毒包膜与细胞质膜融合的特殊细胞介导机制表明,这而非病毒胞饮作用,是仙台病毒感染的机制。

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