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关于细胞膜反应在决定病毒毒力中的作用。副流感病毒SV5在两种细胞类型中的不同作用。

On the role of the response of the cell membrane in determining virus virulence. Contrasting effects of the parainfluenza virus SV5 in two cell types.

作者信息

Holmes K V, Choppin P W

出版信息

J Exp Med. 1966 Sep 1;124(3):501-20. doi: 10.1084/jem.124.3.501.

DOI:10.1084/jem.124.3.501
PMID:4288512
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2138234/
Abstract

The simian myxovirus SV5 multiplies in a continuous line of baby hamster kidney (BHK21-F) cells causing extensive cell fusion, followed by cell death. After inoculation of 15 PFU/cell, the latent period was 7 hr, the doubling time approximately 60 min, and the yield 7 PFU per cell. Giant cell formation began about 6 hr after infection and rapidly progressed to the formation by 14 to 18 hr of a single syncytium which disintegrated by 24 to 36 hr. In contrast, SV5 multiplies in primary rhesus monkey kidney cells for long periods of time producing high yields of virus with little cytopathic effect. High multiplicities of SV5 induced cell fusion in BHK21-F cells within 1 hr in the absence of virus multiplication but had no visible effect on monkey kidney cells. Time-lapse photomicrography has demonstrated that giant cells form by fusion of infected cells, and that some polykaryocytes divide. During aberrant division of polykaryocytes giant nuclei are formed from the nuclear material of several parent nuclei. The cytoplasmic development of viral antigens as demonstrated by immunofluorescence is similar in BHK21-F and monkey kidney cells. Synthesis of cellular DNA, RNA, and protein in monkey kidney cells is not shut off by SV5-infection, and in BHK21-F cells synthesis of these macromolecules is not inhibited until after extensive cell fusion has occurred 12 to 15 hr after infection. Persistently infected BHK21-F and monkey kidney cells have been serially carried through 11 and 28 cell passages, respectively. The results suggest that whether SV5 acts as a moderate virus, as in monkey kidney cells, or a virulent virus, as in BHK21-F cells, depends on the response of the cell membrane to the virus.

摘要

猿猴黏液病毒SV5在连续传代的幼仓鼠肾(BHK21-F)细胞中增殖,导致广泛的细胞融合,随后细胞死亡。以每细胞接种15个空斑形成单位(PFU)后,潜伏期为7小时,倍增时间约为60分钟,每细胞产量为7个PFU。感染后约6小时开始形成巨细胞,并在14至18小时迅速发展为形成单个多核体,该多核体在24至36小时解体。相比之下,SV5可在原代恒河猴肾细胞中长时间增殖,产生高滴度病毒,且细胞病变效应很小。高滴度的SV5在无病毒增殖的情况下,1小时内在BHK21-F细胞中诱导细胞融合,但对猴肾细胞无明显影响。延时显微摄影表明,巨细胞由受感染细胞融合形成,且一些多核细胞会分裂。在多核细胞异常分裂过程中,巨大核由几个亲代核的核物质形成。通过免疫荧光显示,病毒抗原在BHK21-F细胞和猴肾细胞中的胞质发育相似。SV5感染不会使猴肾细胞中的细胞DNA、RNA和蛋白质合成停止,而在BHK21-F细胞中,这些大分子的合成直到感染后12至15小时发生广泛细胞融合后才受到抑制。持续感染的BHK21-F细胞和猴肾细胞分别连续传代了11代和28代。结果表明,SV5是像在猴肾细胞中那样表现为温和病毒,还是像在BHK21-F细胞中那样表现为强毒病毒,取决于细胞膜对病毒的反应。

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On the role of the response of the cell membrane in determining virus virulence. Contrasting effects of the parainfluenza virus SV5 in two cell types.关于细胞膜反应在决定病毒毒力中的作用。副流感病毒SV5在两种细胞类型中的不同作用。
J Exp Med. 1966 Sep 1;124(3):501-20. doi: 10.1084/jem.124.3.501.
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Mechanism of Polykaryocytosis Associated with Noncytopathic Infection by Measles Virus.麻疹病毒非细胞病变感染相关的多核细胞增多机制
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