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首页> 外文期刊>Journal of Virology >Accumulation and breakdown of RNA-deficient intracellular virus particles in interferon-treated NIH 3T3 cells chronically producing Moloney murine leukemia virus.
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Accumulation and breakdown of RNA-deficient intracellular virus particles in interferon-treated NIH 3T3 cells chronically producing Moloney murine leukemia virus.

机译:在干扰素处理的NIH 3T3细胞中的RNA缺陷细胞内病毒颗粒的累积和分解长期产生摩尼鼠白血病病毒。

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Interferon treatment of NIH 3T3 cells chronically infected with Moloney murine leukemia virus inhibited about 95% of virus release. This inhibition was accompanied by a three- to twofold accumulation of intracellular virions. However, this accumulation could be demonstrated only be exogenous reverse transcriptase reaction assay or radioactive labeling of the assembled viral proteins. It could not be shown by the endogenous reverse transcriptase reaction assay, which depended on endogenous viral RNA, or by labeling the encapsidated viral RNA. It was therefore evident that most of the intracellular virions accumulated in interferon-treated cells were RNA deficient. Hybridization analysis revealed that these virions were deficient of genomic viral RNA, whereas size analysis by gel electrophoresis suggested that the deficiency of 4S RNA normally packaged in Moloney murine leukemia virus was even stronger. Our data also suggested that this RNA deficiency was not due to degradation of the encapsidated RNA, but more likely to a defect in virus assembly. RNA-lacking intracellular virions were unstable; they were found to collapse before being released.
机译:NIH 3T3细胞的干扰素治疗慢性感染莫尼鼠白血病病毒抑制了约95%的病毒释放。该抑制伴有细胞内病毒藻的三个两倍。然而,可以证明该积累仅是外源性逆转录酶反应测定或组装病毒蛋白的放射性标记。内源性逆转录酶反应测定不能显示,其依赖于内源性病毒RNA,或通过标记包封的病毒RNA。因此,显而易见的是,在干扰素处理的细胞中积聚的大多数细胞内病毒中缺乏RNA缺陷。杂交分析表明,这些病毒粒子缺乏基因组病毒RNA,而凝胶电泳的尺寸分析表明,在莫尼鼠白血病病毒中通常包装的4S RNA缺乏甚至更强。我们的数据还表明,这种RNA缺乏症不是由于封装的RNA的降解,但更可能在病毒组件中的缺陷。 RNA缺乏细胞内病毒藻是不稳定的;在被释放之前,他们被发现崩溃。

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