Suppr超能文献

小鼠胚胎细胞中干扰素依赖性流感病毒抗性的表达

Expression of interferon dependent resistance to influenza virus in mouse embryo cells.

作者信息

Arnheiter H, Staeheli P

出版信息

Arch Virol. 1983;76(2):127-37. doi: 10.1007/BF01311696.

Abstract

Adult but not newborn mice bearing the allele M chi display a specific resistance to in vivo infection with orthomyxoviruses. In vitro, cells isolated from adult M chi-animals exhibit a several hundred-fold higher sensitivity to the action of interferon (IFN) against influenza viruses than do cells from M chi-negative mice. We here tested whether or not cells from immature M chi-bearing animals would likewise express the virus-specific higher sensitivity to IFN. Cultured cells from 16-day gestation mouse embryos with and without M chi were equally permissive for an influenza virus when single cycle virus growth was measured. However, influenza virus plaques were smaller in M chi-cells. Treatment of cells with mouse interferon reduced viral protein synthesis, single cycle virus yields and the number of virus plaques more efficiently in M chi-cells than in non-M chi-cells. The smaller size of influenza virus plaques in M chi-cells not treated with IFN seems to be due to the action of endogenous IFN:inclusion of anti-interferon antibodies in the agar overlay during plaque formation resulted in plaques of approximately the size seen in control cells. When treated with the same dose of IFN, cells with M chi developed protection against influenza virus more rapidly than cells without M chi. However, after removal of IFN, the antiviral protection decayed more rapidly in cells in cells without M chi. No differences in sensitivity to IFN, viral plaque formation and kinetics of induction and decay of the antiviral state were observed between the two cell types when the rhabdovirus VSV was used as challenge. Thus, the allele M chi is expressed in cultured embryo cells much as in cells from adult animals, and susceptibility of newborn M chi-animals to influenza virus infection cannot be due to inability of their cells to respond to IFN appropriately.

摘要

携带等位基因M chi的成年小鼠而非新生小鼠对正粘病毒的体内感染具有特异性抗性。在体外,从成年M chi动物分离的细胞对干扰素(IFN)抗流感病毒作用的敏感性比来自M chi阴性小鼠的细胞高数百倍。我们在此测试了来自携带M chi的未成熟动物的细胞是否同样会表现出对IFN的病毒特异性更高敏感性。在测量单周期病毒生长时,来自妊娠16天的有或没有M chi的小鼠胚胎的培养细胞对流感病毒同样敏感。然而,M chi细胞中的流感病毒蚀斑较小。用小鼠干扰素处理细胞时,与非M chi细胞相比,M chi细胞中病毒蛋白合成、单周期病毒产量和病毒蚀斑数量的降低更为有效。未用IFN处理的M chi细胞中流感病毒蚀斑较小似乎是由于内源性IFN的作用:在蚀斑形成过程中在琼脂覆盖物中加入抗干扰素抗体导致蚀斑大小与对照细胞中所见的大致相同。当用相同剂量的IFN处理时,携带M chi的细胞比不携带M chi的细胞更快地产生对流感病毒的保护作用。然而,去除IFN后,不携带M chi的细胞中抗病毒保护作用的衰减更快。当用弹状病毒VSV作为攻击病毒时,两种细胞类型在对IFN的敏感性、病毒蚀斑形成以及抗病毒状态的诱导和衰减动力学方面均未观察到差异。因此,等位基因M chi在培养的胚胎细胞中的表达与成年动物细胞中的表达非常相似,新生M chi动物对流感病毒感染的易感性不能归因于其细胞无法对IFN作出适当反应。

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