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人胚成纤维细胞对柯萨奇病毒B3的易感性。体外病毒遗传标记及免疫金复型技术对病毒受体分布定位的研究

Permissiveness of human embryonal fibroblasts for coxsackieviruses B3. Investigations on virus genetic markers in vitro and localization of virus receptor distribution by immunogold replica technique.

作者信息

Tonew M, Wagner B, Wagner M, Schmidtke M, Stelzner A

机构信息

Hans-Knöll-Institute for Natural Product Research, Jena, Germany.

出版信息

Zentralbl Bakteriol. 1996 Jul;284(2-3):443-56. doi: 10.1016/s0934-8840(96)80118-6.

Abstract

In our previous paper (29) we could show, that the replication of four Coxsackie B3 virus strains in human fibroblast lines from different origin was dependent on both the virus strain and the cell line used. Although generally no cytopathic effect could be observed out of one virus strain more pathogenic virus variants could be selected able to destroy virus-sensitive as well as insensitive fibroblasts. The present study was designed to characterize these virus strains by using several in vitro genetic markers. Differences were found concerning plaque size and the temperature marker, whereas the other markers (d, DD, DEAE-D) remained constant. Furthermore, these models of persistent as well as lytic CVB3 infection were analysed by immunoelectron microscopy to study the interaction of viral ligands with cellular receptors. The qualitative and quantitative differences in adsorption of the CVB3 strains to two human fibroblast lines as well as to HeLa cells corresponded well with the virological results. They underline that even in vitro in human cell lines of different origin changes in distribution, quantity and quality of receptors were demonstrable forming the base for the various virus sensitivity.

摘要

在我们之前的论文(29)中,我们能够证明,四种柯萨奇B3病毒株在源自不同来源的人成纤维细胞系中的复制取决于所用的病毒株和细胞系。尽管通常从一种病毒株中观察不到细胞病变效应,但可以选择出更具致病性的病毒变体,它们能够破坏对病毒敏感以及不敏感的成纤维细胞。本研究旨在通过使用几种体外遗传标记来表征这些病毒株。在蚀斑大小和温度标记方面发现了差异,而其他标记(d、DD、DEAE-D)保持不变。此外,通过免疫电子显微镜分析了这些持续性以及溶解性柯萨奇B3病毒感染的模型,以研究病毒配体与细胞受体的相互作用。柯萨奇B3病毒株对两种人成纤维细胞系以及对HeLa细胞吸附的定性和定量差异与病毒学结果非常吻合。它们强调,即使在体外不同来源的人细胞系中,受体的分布、数量和质量的变化也是可证明的,这构成了各种病毒敏感性的基础。

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