Detjen B M, Jen G, Thach R E
J Virol. 1981 May;38(2):777-81. doi: 10.1128/JVI.38.2.777-781.1981.
Superinfection with poliovirus of HeLa cells already infected with encephalomyocarditis (EMC) virus does not inhibit translation of EMC viral mRNA, whereas residual host translation is completely inhibited. This result indicates that the cap recognition factors inactivated by poliovirus are not required for translation of EMC viral mRNA in vivo, in agreement with previous in vitro experiments. This raises the question of why EMC virus has evolved a capindependent translation mechanism.
已经感染脑心肌炎（EMC）病毒的HeLa细胞再感染脊髓灰质炎病毒，并不会抑制EMC病毒mRNA的翻译，而宿主细胞的残余翻译则会被完全抑制。这一结果表明，脊髓灰质炎病毒使其失活的帽识别因子在体内对EMC病毒mRNA的翻译并非必需，这与之前的体外实验结果一致。这就引发了一个问题，即为什么EMC病毒进化出了一种不依赖帽的翻译机制。
