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在无病毒增殖情况下,缺陷干扰流感病毒干扰活性的细胞内稳定性

Intracellular stability of the interfering activity of a defective interfering influenza virus in the absence of virus multiplication.

作者信息

Cane C, McLain L, Dimmock N J

出版信息

Virology. 1987 Aug;159(2):259-64. doi: 10.1016/0042-6822(87)90463-6.

Abstract

Half-lives of the interfering activity of a human defective interfering (DI) influenza virus and of viral RNA in MDCK cells inoculated with noninfectious DI virus were 25 and 17 days, respectively, and of viral RNA in cells inoculated with noninfectious uv-irradiated standard virus was 21 days. In neither case was there evidence of virus replication (de novo synthesis of viral proteins, haemagglutinin, or infectivity). The half-life in BHK cells was shorter, although still considerable, showing evidence of a host contribution to stability. Implications of the putative persistence of influenza virus genes in vivo to the natural history of the virus are discussed.

摘要

在接种无感染性缺陷干扰(DI)流感病毒的MDCK细胞中,人缺陷干扰流感病毒干扰活性的半衰期和病毒RNA的半衰期分别为25天和17天;在接种无感染性紫外线照射标准病毒的细胞中,病毒RNA的半衰期为21天。在这两种情况下均未发现病毒复制的证据(病毒蛋白、血凝素的从头合成或感染性)。在BHK细胞中的半衰期较短,尽管仍然可观,这表明宿主对稳定性有贡献。文中讨论了流感病毒基因在体内可能的持续存在对病毒自然史的影响。

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