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细胞松弛素D加速新城疫病毒从受感染细胞中的释放。

Cytochalasin D accelerates the release of Newcastle disease virus from infected cells.

作者信息

Morrison T G, McGinnes L J

出版信息

Virus Res. 1985 Dec;4(1):93-106. doi: 10.1016/0168-1702(85)90023-1.

Abstract

The role of the cellular cytoskeleton in Newcastle disease virus (NDV) infection was explored in two ways. First, the extent of the association of viral proteins with the cytoskeletal fraction of chicken embryo cells was determined. NDV-infected cells, pulse-labelled with [35S]methionine with or without a subsequent chase, were fractionated into Triton X-100-soluble and cytoskeletal fractions. All NDV proteins become associated with the cytoskeletal fraction of cells subsequent to their synthesis. Mixing experiments provided evidence against nonspecific sticking of proteins with this cell fraction. Second, the functional significance of the cytoskeletal association was explored using the inhibitor cytochalasin D. In the presence of this inhibitor, the rate of release of radioactively labelled virions was accelerated 2.5-fold. Colchicine did not significantly alter the rate of virion release. Virus particles released from cytochalasin D-treated cells had the same density as virions released from untreated cells, but were slightly less infectious and contained less actin. These results suggest that functional microfilaments do not play an obligatory role in viral morphogenesis but rather function to slow virus particle release.

摘要

通过两种方式探究了细胞细胞骨架在新城疫病毒(NDV)感染中的作用。首先,确定了病毒蛋白与鸡胚细胞细胞骨架部分的结合程度。用[35S]甲硫氨酸脉冲标记感染NDV的细胞,无论随后有无追踪,将其分为Triton X-100可溶性部分和细胞骨架部分。所有NDV蛋白在合成后都会与细胞的细胞骨架部分结合。混合实验提供了证据,证明蛋白质与该细胞部分不存在非特异性黏附。其次,使用细胞松弛素D抑制剂探究了细胞骨架结合的功能意义。在该抑制剂存在的情况下,放射性标记病毒粒子的释放速率加快了2.5倍。秋水仙碱并未显著改变病毒粒子的释放速率。从经细胞松弛素D处理的细胞中释放的病毒粒子与从未经处理的细胞中释放的病毒粒子密度相同,但感染性略低且所含肌动蛋白较少。这些结果表明,功能性微丝在病毒形态发生中不发挥必需作用,而是起到减缓病毒粒子释放的作用。

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