Wall R, Taylor M W
J Virol. 1969 Nov;4(5):681-7. doi: 10.1128/JVI.4.5.681-687.1969.
Mengovirus infection of a restrictive cell line, Maden's bovine kidney (MDBK), results in a virus yield 1,000-fold less than that obtained from productively infected cell lines such as L cells or Ehrlich ascites tumor cells (EAT). Cells of both types of host systems are infected with comparable efficiencies and are completely killed as a consequence of infection. Infective center assays, coupled with the observation of total cell killing, suggest that comparable numbers of cells synthesize viral antigen and release virus in both types of host system. Viral-specific ribonucleic acid (RNA) synthesis is initiated and proceeds in an identical fashion for approximately 4 hr after the infection of MDBK, EAT, or L-cells. At this time, viral RNA synthesis in MDBK ceases, whereas viral RNA synthesis in EAT and L-cells continues at a linear rate. These results indicate that none of the early viral events leading to the initiation of viral-specific RNA synthesis constitutes the primary site of mengovirus restriction in MDBK. Rather it appears that the cessation of viral RNA synthesis in restrictive cells constitutes the primary limiting event. Based on its delayed interaction with mengovirus RNA synthesis, it appears that the host-related restrictive agent is initially compartmentalized and then released as a consequence of infection subsequent to those early events in mengovirus infection leading to the initiation and continued synthesis of viral RNA.
脑心肌炎病毒感染一种限制性细胞系——马登氏牛肾细胞(MDBK),产生的病毒产量比从诸如L细胞或艾氏腹水瘤细胞(EAT)等能有效感染的细胞系中获得的产量少1000倍。两种宿主系统的细胞被感染的效率相当,并且感染后都会完全死亡。感染中心测定,结合对细胞全部死亡的观察,表明在两种宿主系统中,合成病毒抗原并释放病毒的细胞数量相当。在MDBK、EAT或L细胞感染后,病毒特异性核糖核酸(RNA)合成开始,并以相同方式进行约4小时。此时,MDBK中的病毒RNA合成停止,而EAT和L细胞中的病毒RNA合成以线性速率继续。这些结果表明,导致病毒特异性RNA合成起始的早期病毒事件均不是脑心肌炎病毒在MDBK中受限的主要位点。相反,似乎限制性细胞中病毒RNA合成的停止构成了主要的限制事件。基于其与脑心肌炎病毒RNA合成的延迟相互作用,宿主相关的限制因子似乎最初是分隔的,然后在脑心肌炎病毒感染中那些导致病毒RNA起始和持续合成的早期事件之后,由于感染而释放。