Katze M G, Chen Y T, Krug R M
Cell. 1984 Jun;37(2):483-90. doi: 10.1016/0092-8674(84)90378-7.
Influenza virus-specific proteins are synthesized at essentially the same levels in late adenovirus-infected HeLa cells as in cells not infected with adenovirus, indicating that influenza viral mRNA escapes the blocks exerted by adenovirus against host-cell mRNA expression-transport from the nucleus and translation. A significant proportion of the influenza viral mRNAs synthesized in these cells possesses the 5' ends of the major late adenovirus transcripts, resulting from capped RNA-primed initiation of influenza viral mRNA synthesis. We determined whether the ability of influenza viral mRNA to escape from the adenovirus-imposed blocks is due to utilization of the adenovirus-specific transport and translational systems because of the adenovirus 5' ends on the influenza viral mRNAs, or to establishment of influenza virus-specific transport and translational systems. Our results indicate that the second mechanism is operating, as the transport of influenza viral mRNAs from the nucleus and their translation is independent of the presence of adenovirus 5' ends. Furthermore, efficient translation of influenza viral mRNAs, but not of either adenovirus or host mRNAs, occurs in cells infected by the adenovirus deletion mutant dl331 , which does not synthesize VAI RNA ( Thimmappaya et al., 1982). Consequently, utilizing the translational machinery that had been inactivated by adenovirus, influenza virus establishes a system that selectively translates influenza viral mRNAs.
在腺病毒感染后期的HeLa细胞中,流感病毒特异性蛋白的合成水平与未感染腺病毒的细胞基本相同,这表明流感病毒mRNA逃脱了腺病毒对宿主细胞mRNA表达(从细胞核转运及翻译)施加的阻碍。在这些细胞中合成的相当一部分流感病毒mRNA具有腺病毒主要晚期转录本的5'端,这是由加帽RNA引发的流感病毒mRNA合成起始导致的。我们确定了流感病毒mRNA逃脱腺病毒施加阻碍的能力是由于流感病毒mRNA上的腺病毒5'端利用了腺病毒特异性转运和翻译系统,还是由于建立了流感病毒特异性转运和翻译系统。我们的结果表明是后一种机制在起作用,因为流感病毒mRNA从细胞核的转运及其翻译与腺病毒5'端的存在无关。此外,在被腺病毒缺失突变体dl331感染的细胞中(该突变体不合成VAI RNA,Thimmappaya等人,1982年),流感病毒mRNA能高效翻译,但腺病毒或宿主mRNA均不能,因此,流感病毒利用被腺病毒灭活的翻译机制,建立了一个选择性翻译流感病毒mRNA的系统。