Lawrence C, Thach R E
J Virol. 1974 Sep;14(3):598-610. doi: 10.1128/JVI.14.3.598-610.1974.
Mouse plasmacytoma ascites tumor cells (MOPC 460) were efficiently infected with encephalomyocarditis virus. Inhibition of host protein synthesis was evident after 2 h and complete by 4 h postinfection. The mechanism by which virus infection results in inhibition of host cell protein synthesis was studied in vitro. Cell-free protein-synthesizing systems, prepared from uninfected and infected cells, were found to be equally active with respect to their abilities to translate cellular and viral mRNAs. The plasmacytoma cell-free system was also shown to be insensitive to the addition of double-stranded viral RNA. Host cellular mRNA was isolated from uninfected and infected cells. No difference in the amount or size distribution of the mRNA was detected. However, the mRNA from infected cells was translated only 46 to 49% as actively as that from uninfected cells. mRNA isolated from cells in which initiation of protein synthesis was inhibited with pactamycin was similarly inactivated. Simultaneous addition of viral RNA and cellular mRNA to the plasmacytoma cell-free system resulted in a complete suppression of the translation of the cellular message, whereas viral RNA was translated normally.
小鼠浆细胞瘤腹水肿瘤细胞（MOPC 460）被脑心肌炎病毒有效感染。感染后2小时宿主蛋白合成受到明显抑制，4小时后完全抑制。在体外研究了病毒感染导致宿主细胞蛋白合成抑制的机制。从未感染和感染细胞制备的无细胞蛋白合成系统在翻译细胞和病毒mRNA的能力方面表现出同等活性。浆细胞瘤无细胞系统也显示对双链病毒RNA的添加不敏感。从未感染和感染细胞中分离出宿主细胞mRNA。未检测到mRNA的量或大小分布有差异。然而，感染细胞的mRNA翻译活性仅为未感染细胞的46%至49%。从用嘌呤霉素抑制蛋白合成起始的细胞中分离的mRNA同样失活。将病毒RNA和细胞mRNA同时添加到浆细胞瘤无细胞系统中导致细胞信息的翻译完全受到抑制，而病毒RNA正常翻译。
