Korant B, Chow N, Lively M, Powers J
Proc Natl Acad Sci U S A. 1979 Jun;76(6):2992-5. doi: 10.1073/pnas.76.6.2992.
Previous studies have shown that primary cleavages in nascent picornavirus precursors are accomplished by cellular proteases. This study has characterized the enzyme in infected cells that produces the capsid polypeptides by secondary cleavages of viral precursors. The kinetics of the production of protease activity correlate with the time course of virus protein synthesis, and the new enzyme has characteristic pH and temperature optima. Guanidine and cycloheximide, which are inhibitors of virus RNA and protein synthesis, prevent production of the protease. As determined by introduction of amino acid analogs into the protease or inhibition by a leucyl chloromethyl ketone, the enzyme is synthesized at a time of infection when host cell proteins are not produced, and the enzyme copurified with a 40,000-dalton virus polypeptide present in the cytoplasm of infected cells. Wild-type levels of protease activity are produced by viral mutants that are defective in coat protein synthesis. The conclusion is that a non-structural poliovirus gene product participates in protein cleavages that produce the viral coat proteins.
先前的研究表明,新生微小核糖核酸病毒前体中的一级切割是由细胞蛋白酶完成的。本研究已对感染细胞中通过病毒前体的二级切割产生衣壳多肽的酶进行了特性描述。蛋白酶活性产生的动力学与病毒蛋白质合成的时间进程相关,并且这种新酶具有特定的最适pH值和温度。胍和环己酰亚胺是病毒RNA和蛋白质合成的抑制剂,它们可阻止蛋白酶的产生。通过将氨基酸类似物引入蛋白酶或用亮氨酰氯甲基酮进行抑制来确定,该酶是在感染时合成的,此时宿主细胞蛋白质并未产生,并且该酶与存在于感染细胞胞质中的一种40,000道尔顿的病毒多肽共纯化。衣壳蛋白合成有缺陷的病毒突变体可产生野生型水平的蛋白酶活性。结论是,一种非结构脊髓灰质炎病毒基因产物参与了产生病毒衣壳蛋白的蛋白质切割过程。