Klessig D F, Anderson C W
J Virol. 1975 Dec;16(6):1650-68. doi: 10.1128/JVI.16.6.1650-1668.1975.
The block to adenovirus 2 (Ad2) multiplication in monkey cells can be overcome by coinfection with simian virus 40 (SV40). To identify this block we have compared the synthesis of Ad2 proteins in monkey cells infected with Ad2 alone (unenhanced) or with Ad2 plus SV40 (enhanced). Synthesis of viral proteins in enhanced cells was virtually identical to that found for permissive infection of human cells by Ad2 alone. In contrast, the unenhanced cells were strikingly deficient in the production of the IV (fiber) and 11.5K proteins whereas the synthesis of 100K and IVa2 was normal. Synthesis of a number of other proteins such as II, V, and P-VII was partially reduced. A similar specific reduction in synthesis of these proteins was found when their messages were assayed by cell-free translation. This result suggests that the block to Ad2 protein synthesis is at the RNA level rather than with the translational machinery of monkey cells. Analysis of the complexity and the concentration of Ak2-specific RNAs, using hybridization of restriction endonuclease fragments of the Ad2 genome to increasing concentrations of RNA, shows that although all species of late Ad2 mRNA are present, the concentration of several species is reduced sevenfold or more in unenhanced monkey cells as compared with enhanced cells. These species come from regions of the genome known to encode the deficient proteins. A model for the failure of adenovirus to multiply in monkey cells, based on abnormal processing of specific adenovirus messages, is presented.
腺病毒2型(Ad2)在猴细胞中的增殖障碍可通过与猿猴病毒40(SV40)共感染来克服。为了确定这一障碍,我们比较了单独感染Ad2(未增强)或同时感染Ad2和SV40(增强)的猴细胞中Ad2蛋白的合成情况。增强细胞中病毒蛋白的合成与单独用Ad2感染人细胞的允许性感染中发现的情况几乎相同。相比之下,未增强的细胞在IV(纤维)和11.5K蛋白的产生上明显不足,而100K和IVa2的合成正常。其他一些蛋白如II、V和P-VII的合成部分减少。当通过无细胞翻译检测这些蛋白的信使核糖核酸时,发现这些蛋白的合成也有类似的特异性减少。这一结果表明,Ad2蛋白合成的障碍发生在RNA水平,而不是在猴细胞的翻译机制上。利用Ad2基因组的限制性内切酶片段与浓度不断增加的RNA杂交,对Ad2特异性RNA的复杂性和浓度进行分析,结果显示,尽管所有种类的Ad2晚期信使核糖核酸都存在,但与增强细胞相比,未增强的猴细胞中几种信使核糖核酸的浓度降低了七倍或更多。这些信使核糖核酸来自基因组中已知编码缺失蛋白的区域。本文提出了一个基于特定腺病毒信使核糖核酸异常加工的腺病毒在猴细胞中无法增殖的模型。