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热灭活的蛙病毒3以时间类别依赖性方式选择性抑制1型马疱疹病毒的翻译。

Heat-inactivated frog virus 3 selectively inhibits equine herpesvirus type 1 translation in a temporal class-dependent manner.

作者信息

Chinchar V G, Caughman G B

出版信息

Virology. 1986 Jul 30;152(2):466-71. doi: 10.1016/0042-6822(86)90149-2.

Abstract

Superinfection of equine herpesvirus type 1 (EHV-1)-infected rabbit kidney cells with heat-inactivated frog virus 3 (delta FV3) differentially blocked EHV-1 protein synthesis. The extent of inhibition varied with the specific EHV-1 message, but in general late protein synthesis was inhibited more than early and immediate early translation. Since FV3 has been shown to block heterologous RNA and protein synthesis, it was necessary to determine whether the observed reduction in herpesvirus protein synthesis was primarily due to a block in translation or to an earlier inhibition of EHV-1 mRNA synthesis. To distinguish between these alternatives, replicate cultures of EHV-1 infected cells were either superinfected with delta FV3 or treated with 10 micrograms/ml actinomycin D at 6 hr after infection, and EHV-1 protein synthesis monitored 3 hr later. We found that addition of actinomycin D to EHV-1 infected cultures had only a slight effect on EHV-1 translation, whereas superinfection with delta FV3 markedly reduced EHV-1 protein synthesis. This result suggested that the observed decline in EHV-1 protein synthesis was not due to the inhibition of herpesvirus mRNA synthesis. In addition, we showed that RNA extracted from delta FV3-superinfected cells directed the synthesis of full-size EHV-1 proteins in vitro indicating that shut-off was not caused by the degradation of EHV-1 mRNAs. Taken together these results show that delta FV3 selectively inhibited EHV-1 protein synthesis and are consistent with earlier observations which suggest that translational shut-off occurs at initiation.

摘要

用热灭活的蛙病毒3(δFV3)对感染1型马疱疹病毒(EHV-1)的兔肾细胞进行双重感染,可差异性地阻断EHV-1蛋白合成。抑制程度因特定的EHV-1信息而异,但总体而言,晚期蛋白合成比早期和极早期翻译受到的抑制更大。由于FV3已被证明可阻断异源RNA和蛋白合成,因此有必要确定观察到的疱疹病毒蛋白合成减少主要是由于翻译受阻还是由于EHV-1 mRNA合成的更早抑制。为了区分这些可能性,在感染后6小时,将EHV-1感染细胞的重复培养物用δFV3进行双重感染或用10微克/毫升放线菌素D处理,并在3小时后监测EHV-1蛋白合成。我们发现,向EHV-1感染培养物中添加放线菌素D对EHV-1翻译只有轻微影响,而用δFV3双重感染则显著降低EHV-1蛋白合成。这一结果表明,观察到的EHV-1蛋白合成下降不是由于疱疹病毒mRNA合成受到抑制。此外,我们表明,从δFV3双重感染细胞中提取的RNA在体外指导全长EHV-1蛋白的合成,这表明关闭不是由EHV-1 mRNA的降解引起的。这些结果综合起来表明,δFV3选择性地抑制EHV-1蛋白合成,并且与早期观察结果一致,即翻译关闭发生在起始阶段。

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