水泡性口炎病毒感染细胞中干扰素的产生及对宿主合成的抑制作用。
Interferon production and inhibition of host synthesis in cells infected with vesicular stomatitis virus.
作者信息
Wertz G W, Youngner J S
出版信息
J Virol. 1970 Oct;6(4):476-84. doi: 10.1128/JVI.6.4.476-484.1970.
Abstract
Infection of L cells with wild-type (L(1)) vesicular stomatitis virus at high or low multiplicities does not result in the production of interferon; however, infection of L cells with low multiplicities of a small-plaque mutant (S(2)) results in the synthesis of large amounts of interferon. In chick embryo (CE) cells, both viruses induce synthesis of interferon; there is no significant multiplicity effect in CE cells. The rate and efficiency of shutoff of macromolecular synthesis in the different host cells is a critical factor in determining the ability of the viruses to induce interferon synthesis. If host ribonucleic acid or protein synthesis is shut off by the virus before the required new ribonucleic acid is transcribed or translated, interferon production does not occur. The relative yield of the two viruses in CE and L cells is not related to the effects of interferon produced during the course of infection.
摘要
用高或低感染复数的野生型（L(1)）水泡性口炎病毒感染L细胞不会产生干扰素；然而，用低感染复数的小斑突变体（S(2)）感染L细胞会导致大量干扰素的合成。在鸡胚（CE）细胞中，两种病毒都诱导干扰素的合成；在CE细胞中没有明显的感染复数效应。不同宿主细胞中大分子合成的关闭速率和效率是决定病毒诱导干扰素合成能力的关键因素。如果在所需的新核糖核酸被转录或翻译之前，宿主核糖核酸或蛋白质合成被病毒关闭，就不会产生干扰素。这两种病毒在CE细胞和L细胞中的相对产量与感染过程中产生的干扰素的作用无关。
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