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含肌动蛋白的微丝在单纯疱疹病毒诱导的细胞病理学中的作用及糖基化抑制剂的影响。

Involvement of actin-containing microfilaments in HSV-induced cytopathology and the influence of inhibitors of glycosylation.

作者信息

Heeg U, Dienes H P, Müller S, Falke D

出版信息

Arch Virol. 1986;91(3-4):257-70. doi: 10.1007/BF01314285.

Abstract

Two and a half hours after infection with a high dose of different strains of HSV-1 which induce rounding of cells, breakdown of actin containing microfilaments can be observed. At the periphery of the cell, actin containing knob-like protuberances were visible. Later on, actin seems to be located exclusively on the surface of cells. Observations were done by immunofluorescence microscopy, scanning electron-microscopy and immunoperoxidase staining of ultrathin sections. The envelope of HSV appears to be stained by anti-actin. Strain IES produces rounding of cells at a high dose of infection before fusion proceeds at 37 degrees C. Similar alterations were not observed with the fusing strains MP and HFEM. Incubation of infected cells at 39 degrees C revealed strain dependent differences of the fusion activity. At 41 degrees C no "fusion from within" of cells but only rounding was detectable. Application of tunicamycin resulted in complete inhibition of fusion by all strains. The fusion activity of some strains of HSV-1 (ANG, HFEM, and MP) was not inhibited by addition of 2-deoxy-D-glucose and 2-fluoro-deoxy-D-glucose. A variant from strain MP could be isolated, which is sensitive to the effects of 2-deoxy-D-glucose. Inhibitors of processing of glycoproteins did not affect fusion of cells.

摘要

用高剂量不同株单纯疱疹病毒1型(HSV-1)感染细胞,两小时半后细胞出现变圆,可观察到含肌动蛋白的微丝断裂。在细胞周边,可见含肌动蛋白的瘤状突起。之后,肌动蛋白似乎仅位于细胞表面。通过免疫荧光显微镜、扫描电子显微镜及超薄切片免疫过氧化物酶染色进行观察。HSV的包膜似乎可被抗肌动蛋白染色。IES株在高剂量感染时,在37℃融合发生前会使细胞变圆。融合株MP和HFEM未观察到类似变化。在39℃孵育感染细胞,显示出融合活性的株系依赖性差异。在41℃,未检测到细胞“自内融合”,仅观察到细胞变圆。衣霉素的应用导致所有株系的融合完全被抑制。添加2-脱氧-D-葡萄糖和2-氟脱氧-D-葡萄糖不会抑制某些HSV-1株系(ANG、HFEM和MP)的融合活性。可从MP株系中分离出一种对2-脱氧-D-葡萄糖作用敏感的变体。糖蛋白加工抑制剂不影响细胞融合。

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