Benavente J, Shatkin A J
Center for Advanced Biotechnology and Medicine, Piscataway, NJ 08855-0759.
Proc Natl Acad Sci U S A. 1988 Jun;85(12):4257-61. doi: 10.1073/pnas.85.12.4257.
Avian reovirus S1133 penetrates and uncoats in suspension cultures of mouse L cells. The multiple species of viral transcripts are produced in the cytoplasm of the infected cell, but they fail to associate with polysomes, consistent with the absence of viral protein synthesis. The selective block in avian virus mRNA translation is not overcome by coinfection with mammalian reovirus type 3, which replicates in mouse L cells, or by hypertonic shock or exposure to a low concentration of cycloheximide. Although the avian viral transcripts are inactive in vivo, RNA extracted from infected, nonpermissive L cells directs the synthesis of a normal spectrum of viral proteins in rabbit reticulocyte lysates. These results indicate that avian viral transcription is not restricted in mouse cells and that viral replication is prevented at the level of initiation of protein synthesis.
禽呼肠孤病毒S1133在小鼠L细胞的悬浮培养物中穿透并脱壳。多种病毒转录本在受感染细胞的细胞质中产生,但它们无法与多核糖体结合,这与病毒蛋白合成的缺失一致。与在小鼠L细胞中复制的哺乳动物呼肠孤病毒3型共感染、高渗休克或暴露于低浓度环己酰亚胺均不能克服禽病毒mRNA翻译的选择性阻断。尽管禽病毒转录本在体内无活性,但从受感染的、非允许性L细胞中提取的RNA可在兔网织红细胞裂解物中指导合成正常谱的病毒蛋白。这些结果表明,禽病毒转录在小鼠细胞中不受限制,并且病毒复制在蛋白质合成起始水平被阻止。