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Infectious process of the parvovirus H-1: correlation of protein content, particle density, and viral infectivity.

机译:细小病毒H-1的传染过程:蛋白质含量,颗粒密度和病毒感染性的相关性。

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The infectious particles of the parvovirus H-1 were characterized with respect to protein content, density in CsCl, and specific infectivity. Heavy-full and light-full particles were purified from infected simian virus 40-transformed newborn human kidney (NB) cells and from simian virus 40-transformed hamster kidney (THK) cells. Analysis of the protein content of these particles demonstrated that the ratio of viral protein VP2' to VP2 was the same in heavy-full and light-full particles derived from the same cell line, but differed significantly between the two hosts. However, the infectivity of the particles from each cell line was the same for all four viral species.. Also, in vitro conversion of VP2' to VP2 did not enhance the particle infectivity of either heavy-full or light-full virus. When the fate of input virus was studied with 125I-labeled H-1, the conversion of VP2' to VP2 occurred in a time-dependent manner up to 24 h postinfection. Simultaneous with the proteolytic cleavage, there was a shift in the density of the heavy-full virus to the light-full density. However, protein analysis of the 125I-labeled light-full virus at various times postinfection indicated that they were not enriched in VP2 when compared with heavy-full virus or the total virus population. Thus, the cleavage of VP2' to VP2 is not responsible for the shift in density from heavy-full to light-full virus, and although these events might be required for infection they appear not to be interdependent.
机译:对细胞病毒H-1的感染性颗粒相对于蛋白质含量,CSCL中的密度和特异性感染性表征。从感染的Simian病毒40转化的新生人肾(Nb)细胞和辛安病毒40转化的仓鼠肾脏(THK)细胞均从感染的Simian病毒40-转化的新生儿患者纯化了沉重的和全颗粒。这些颗粒的蛋白质含量的分析表明,病毒蛋白VP2'至VP2的比例在衍生自相同细胞系的重满性和清淡的颗粒中相同,但在两个宿主之间有显着不同。然而,对于所有四种病毒物种,来自每种细胞系的颗粒的感染性也是相同的。此外,VP2'至VP2的体外转化率并未增强重满血或清淡的病毒的颗粒感染性。当用125I标记的H-1进行输入病毒的命运时,VP2'至VP2的转化以时间依赖于24小时,发生在发布中。同时用蛋白水解裂解,在重满性病毒的密度下换换气以光充分密度。然而,与重含量的病毒或总病毒群相比,蛋白质分析了125i标记的光完全病毒,表明它们在VP2中未富集。因此,VP2'至VP2的切割不对密度的偏移较大,虽然可能需要这些事件感染,但它们看起来不依赖。

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  • 来源
    《Journal of Virology》 |1981年第3期|共8页
  • 作者

    P R Paradiso;

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  • 收录信息 美国《科学引文索引》(SCI);
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