McAllister P E, Wagner R R
J Virol. 1976 May;18(2):550-8. doi: 10.1128/JVI.18.2.550-558.1976.
The response of mouse L cells to infection with wild-type (wt) and temperature-sensitive (ts) mutants of vesicular stomatitis virus was monitored by sodium dodecyl sulfate-polyacrylamide gel electrophoresis to delineate the synthesis of host cell and viral proteins. Experiments utilized transcriptase mutants of complementation group I (ts114 and ts13), a group IV mutant (ts44) that is restricted in total RNA synthesis (RNA-1) but not in primary transcription, and a group II mutant (ts52) variably restricted in RNA synthesis (RNA +/-). L cells infected with ts mutants at permissive temperature exhibited the wt response of progressive inhibition of host cell protein synthesis accompanied by accumulation of all five viral proteins. Mutant ts44 (IV) also switched off cell protein synthesis at restrictive temperature and accumulated all five viral proteins, but with disproportionate ratios of N and G proteins. At restrictive temperature, cells infected with group I ts mutants failed to accumulate any viral protein and did not exhibit significant reduction in host cell protein synthesis. These data suggest that vesicular stomatitis virus inhibits cell protein synthesis at a stage of viral infection after transcription and possibly translation but preceding replication of progeny viral RNA.
通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳监测小鼠L细胞对水泡性口炎病毒野生型(wt)和温度敏感型(ts)突变体感染的反应,以描绘宿主细胞和病毒蛋白的合成情况。实验使用了互补组I的转录酶突变体(ts114和ts13)、在总RNA合成(RNA-1)中受限但在初级转录中不受限的IV组突变体(ts44)以及在RNA合成(RNA +/-)中可变受限的II组突变体(ts52)。在允许温度下用ts突变体感染的L细胞表现出野生型反应,即宿主细胞蛋白合成逐渐受到抑制,同时所有五种病毒蛋白积累。突变体ts44(IV)在限制温度下也关闭了细胞蛋白合成并积累了所有五种病毒蛋白,但N和G蛋白的比例不均衡。在限制温度下用I组ts突变体感染的细胞未能积累任何病毒蛋白,宿主细胞蛋白合成也未出现显著减少。这些数据表明,水泡性口炎病毒在病毒感染的转录和可能的翻译之后但在子代病毒RNA复制之前的阶段抑制细胞蛋白合成。