Schrader A P, Westaway E G
Department of Microbiology, Monash University, Clayton, Victoria, Australia.
Arch Virol. 1990;114(1-2):75-89. doi: 10.1007/BF01311013.
Infection with poliovirus effectively inhibited the translation of Vero cell messengers (carrying type 1 or type 2 caps at the 5' end) and of influenza virus messengers (type 1 caps) in co-infections. In contrast, Kunjin virus RNA (type 1 caps) and Semliki Forest virus RNA (a togavirus, with type 0 caps) continued to be translated in the presence of co-infecting poliovirus. Translation of Kunjin virus RNA was also unaffected during co-infections with either influenza virus or Semliki Forest virus. Guanidine treatment effectively blocked poliovirus replication only, but the inhibitory effect on translation of cell messengers and influenza virus messengers was still observed, indicating that this effect was not caused by competition in translation with poliovirus messengers. It was therefore concluded that the observed inhibition was most likely caused by cleavage of the p220 subunit of the cap binding protein (CBP) complex of the cell normally required for translation of capped messengers, as reported by others. However, Kunjin virus RNA could be efficiently translated apparently in the absence of a functional CBP complex, except when its secondary structure was stabilized by hypertonic salt in the culture medium.
脊髓灰质炎病毒感染在共感染时有效抑制了Vero细胞信使核糖核酸（5'端带有1型或2型帽结构）以及流感病毒信使核糖核酸（1型帽结构）的翻译。相比之下，在共感染脊髓灰质炎病毒的情况下，库京病毒核糖核酸（1型帽结构）和塞姆利基森林病毒核糖核酸（一种披膜病毒，0型帽结构）仍能继续翻译。在与流感病毒或塞姆利基森林病毒共感染期间，库京病毒核糖核酸的翻译也不受影响。胍处理仅有效阻断了脊髓灰质炎病毒的复制，但对细胞信使核糖核酸和流感病毒信使核糖核酸翻译的抑制作用仍然存在，这表明这种作用不是由与脊髓灰质炎病毒信使核糖核酸在翻译上的竞争引起的。因此得出结论，如其他人所报道的那样，观察到的抑制作用很可能是由于细胞帽结合蛋白（CBP）复合物的p220亚基被裂解所致，而该复合物是翻译带帽信使核糖核酸通常所需的。然而，库京病毒核糖核酸显然可以在缺乏功能性CBP复合物的情况下有效翻译，除非其二级结构在培养基中因高渗盐而稳定。
