Suppr超能文献

用埃德蒙斯顿麻疹病毒持续缺陷感染的HeLa细胞与Vero细胞共培养后,Vero细胞出现可变感染及同源干扰。

Variable infection of Vero cells and homologous interference after co-cultivation with HeLa cells with persistent defective infection by Edmonston measles virus.

作者信息

Rustigian R, Winston S H, Darlington R W

出版信息

Infect Immun. 1979 Mar;23(3):775-86. doi: 10.1128/iai.23.3.775-786.1979.

Abstract

The HeLa subline K11A-HG-1 (line of HeLa cells persistently infected with Edomonston measles virus but containing little or no transmissible infectious virus) was co-cultivated with Vero cells. Focal syncytia were formed containing measles antigen and accumulations of nucleocapsid-like structures with no detectable production of transmissible infectious virus or positive hemadsorption. The infection aborted between 2 and 3 weeks after preparation of co-cultures. Upon subculture of co-cultures, occasionally complete infections (progressive syncytial degeneration, hemadsorption, and production of transmissible infectious virus) appeared. A linear dose response curve for nontransmissible infection was obtained along with evidence that measles antigen had to be present on the surface of K11A-HG-1 cells for their infectivity for Vero cells. The basis for initiation of Vero cell infection by living K11A-HG-1 cells, but not by nonviable intact K11A-HG-1 cells killed by a virus-preserving technique, nor by disrupted K11A-HG-1 cells, is, at present, a matter of speculation. However, several lines of evidence were obtained which suggested that subsequent development of delayed variable transmissible Vero cell infection occurred because of a type of viral interference, including the presence of an inhibitor in K11A-HG-1 cultures, the bulk of which was cell-associated.

摘要

将HeLa细胞亚系K11A-HG-1(持续感染埃登斯顿麻疹病毒但几乎不含或不含可传播感染性病毒的HeLa细胞系)与Vero细胞共培养。形成了含有麻疹抗原的局灶性合胞体以及核衣壳样结构的聚集物,未检测到可传播感染性病毒的产生或阳性血细胞吸附现象。共培养物制备后2至3周感染终止。对共培养物进行传代培养时,偶尔会出现完全感染(进行性合胞体变性、血细胞吸附以及可传播感染性病毒的产生)。获得了非传播性感染的线性剂量反应曲线,同时有证据表明麻疹抗原必须存在于K11A-HG-1细胞表面才能使其对Vero细胞具有感染性。目前,活的K11A-HG-1细胞能引发Vero细胞感染,而通过病毒保存技术杀死的无活力完整K11A-HG-1细胞以及破碎的K11A-HG-1细胞则不能引发感染,其原因尚属推测。然而,获得了几条证据,表明随后出现延迟性可变可传播Vero细胞感染是由于一种病毒干扰类型,包括K11A-HG-1培养物中存在一种抑制剂,其大部分与细胞相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a0/414233/e1d6ddf64d00/iai00183-0226-a.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验