Fox R I, Baum S G
J Virol. 1972 Aug;10(2):220-7. doi: 10.1128/JVI.10.2.220-227.1972.
The mechanism by which simian virus 40 converts the abortive adenovirus type 7 infection of monkey cells into an efficient lytic infection has been investigated. Analysis of ribonucleic acid (RNA) synthesis during unenhanced and enhanced infection of monkey cells has shown that adenovirus RNA synthesized in the abortive infection contains both "early" and "late" sequences. In hybridization competition experiments, early adenovirus RNA from human cells prevented the hybridization of only 20% of the adenovirus RNA transcribed in unenhanced infection. Further, the RNA from unenhanced cells was able to completely block the hybridization of RNA synthesized during enhanced infection. Finally, virus-associated RNA, which is a late RNA transcribed in lytic adenovirus infection, is also produced in the unenhanced infection. An accompanying paper describes a marked deficiency in adenoviral capsid protein synthesis in the unenhanced infection. We conclude that RNA sequences, which are sufficient to code for the synthesis and assembly of structural proteins of adenovirus, are transcribed but are not efficiently translated in the unenhanced adenovirus infection of monkey cells.
已对猿猴病毒40将猴细胞中腺病毒7型的流产感染转化为高效裂解感染的机制进行了研究。对猴细胞未增强感染和增强感染期间核糖核酸(RNA)合成的分析表明,在流产感染中合成的腺病毒RNA同时包含“早期”和“晚期”序列。在杂交竞争实验中,来自人细胞的早期腺病毒RNA仅阻止了未增强感染中转录的腺病毒RNA的20%的杂交。此外,未增强细胞的RNA能够完全阻断增强感染期间合成的RNA的杂交。最后,病毒相关RNA是在裂解性腺病毒感染中转录的晚期RNA,在未增强感染中也会产生。一篇配套论文描述了未增强感染中腺病毒衣壳蛋白合成的明显缺陷。我们得出结论,足以编码腺病毒结构蛋白合成和组装的RNA序列被转录,但在猴细胞未增强的腺病毒感染中未被有效翻译。