Svitkin Y V, Maslova S V, Agol V I
Virology. 1985 Dec;147(2):243-52. doi: 10.1016/0042-6822(85)90127-8.
In mRNA-dependent extracts of Krebs-2 cells, RNAs from attenuated strains of poliovirus type 1 and type 3 exhibited diminished template activity as compared to RNAs from the respective virulent counterparts. This defect appeared to be due to the impaired initiation of viral polyprotein synthesis as evidenced by a relatively low level of accumulation of polypeptide 1a (which corresponds to an NH2-terminal region of the polyprotein) in samples programmed with RNAs from attenuated strains. In reticulocyte lysates, where poliovirus RNA is translated predominantly from abnormal (internal) sites [Dorner et al. (1984) J. Virol. 50, 507-514], this difference in the overall template activity of the attenuated and virulent poliovirus genomes was less pronounced, but the correct initiation (as judged by polypeptide 1a accumulation) was again more efficient on RNAs from virulent strains. It is suggested that template deficiency is a factor contributing to the attenuated phenotype of poliovirus strains studied. A possible involvement of nucleotide sequences located far upstream from the initiator codon in the control of translation of poliovirus genome is briefly discussed.
在克雷布斯2细胞的mRNA依赖性提取物中,与来自各自强毒株的RNA相比,1型和3型脊髓灰质炎病毒减毒株的RNA表现出降低的模板活性。这种缺陷似乎是由于病毒多聚蛋白合成起始受损所致,这一点可通过在用减毒株RNA编程的样品中多肽1a(对应于多聚蛋白的NH2末端区域)的积累水平相对较低得到证明。在网织红细胞裂解物中,脊髓灰质炎病毒RNA主要从异常(内部)位点进行翻译[多纳等人(1984年)《病毒学杂志》50卷,507 - 514页],减毒和强毒脊髓灰质炎病毒基因组的整体模板活性的这种差异不太明显,但正确起始(通过多肽1a积累判断)在来自强毒株的RNA上再次更有效。有人认为模板缺陷是所研究的脊髓灰质炎病毒株减毒表型的一个促成因素。还简要讨论了位于起始密码子上游很远位置的核苷酸序列在脊髓灰质炎病毒基因组翻译控制中的可能作用。