Miller D K, Lenard J
J Gen Virol. 1982 Jun;60(Pt 2):327-33. doi: 10.1099/0022-1317-60-2-327.
The way in which ultraviolet-irradiated vesicular stomatitis virus (VSV) inhibits the early events in VSV infection has been further characterized. Comparison of several different u.v.-irradiated thermolabile, temperature-sensitive mutants before and after heat inactivation established a requirement for inhibitory activity of functional G, N and L proteins, but not M protein. Defective-interfering (DI) particles, whether irradiated or not, inhibited VSV primary transcription as efficiently as UV-VSV, suggesting that virus proteins rather than transcription products are responsible for inhibition. Addition of inhibitory UV-VSV at different times after infection established that inhibition results from an action at an intracellular site, rather than at the cell surface or in the process of internalization. A similar inhibition by UV-VSV of infection by Sendai virus, Semliki Forest virus, Sindbis virus and influenza virus suggests that UV-VSV is acting by inducing a general change in the intracellular environment.
紫外线照射的水疱性口炎病毒(VSV)抑制VSV感染早期事件的方式已得到进一步的表征。对几种不同的紫外线照射的热不稳定、温度敏感突变体在热灭活前后进行比较,确定了功能性G、N和L蛋白的抑制活性是必需的,但M蛋白不是。缺陷干扰(DI)颗粒,无论是否经过照射,抑制VSV初级转录的效率与紫外线照射的VSV相同,这表明病毒蛋白而非转录产物是抑制的原因。在感染后的不同时间添加抑制性紫外线照射的VSV,确定抑制是由细胞内位点的作用引起的,而不是在细胞表面或内化过程中。紫外线照射的VSV对仙台病毒、Semliki森林病毒、辛德毕斯病毒和流感病毒感染的类似抑制表明,紫外线照射的VSV是通过诱导细胞内环境的普遍变化而起作用的。