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通过感染弗瑞德氏鼠白血病病毒在小鼠体内建立的干扰。

Interference established in mice by infection with Friend murine leukemia virus.

作者信息

Mitchell T, Risser R

机构信息

McArdle Laboratory for Cancer Research, University of Wisconsin-Madison 53706.

出版信息

J Virol. 1992 Sep;66(9):5696-702. doi: 10.1128/JVI.66.9.5696-5702.1992.

Abstract

Retroviral interference is manifested in chronically infected cells as a decrease in susceptibility to superinfection by virions using the same cellular receptor. The pattern of interference reflects the cellular receptor specificity of the chronically infecting retrovirus and is mediated by the viral envelope glycoprotein, which is postulated to bind competitively all cellular receptors available for viral attachment. We established retroviral interference in mice by infecting them with Friend murine leukemia virus and them measured susceptibility to superinfection by challenging the mice with the erythroproliferative spleen focus-forming virus. Infection of approximately 10% of nucleated splenocytes rendered mice 1% as susceptible to superinfection as untreated controls. The magnitude of this effect was the same in mice incapable of producing neutralizing antibodies or genetically deficient for T cells. The results indicated that retroviral interference in vivo was established rapidly with infection of a fraction of the host cell population and that the decrease in susceptibility to superinfection occurred without a detectable contribution by immunologic factors.

摘要

逆转录病毒干扰在慢性感染细胞中表现为,使用相同细胞受体的病毒粒子对重复感染的易感性降低。干扰模式反映了慢性感染逆转录病毒的细胞受体特异性,并且由病毒包膜糖蛋白介导,据推测该蛋白可竞争性结合所有可用于病毒附着的细胞受体。我们通过用弗氏小鼠白血病病毒感染小鼠,在小鼠中建立了逆转录病毒干扰,然后用红细胞增生性脾集落形成病毒攻击小鼠,测定其对重复感染的易感性。约10%的有核脾细胞被感染后,小鼠对重复感染的易感性仅为未处理对照的1%。在无法产生中和抗体或T细胞基因缺陷的小鼠中,这种效应的程度相同。结果表明,体内逆转录病毒干扰在感染一部分宿主细胞群体后迅速建立,并且对重复感染易感性的降低在没有免疫因素可检测贡献的情况下发生。

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