Huang J T, Schneider R J
Kaplan Cancer Center, New York University Medical Center, New York 10016.
Cell. 1991 Apr 19;65(2):271-80. doi: 10.1016/0092-8674(91)90161-q.
Adenovirus (Ad) infection results in a marked inhibition of cellular protein synthesis that initiates during the late phase of the viral infectious cycle. We show that the mechanism used for suppression of cellular protein synthesis during cell cycle progression is exploited by Ad to repress host and enhance late viral mRNA translation. Discrimination between cellular and late Ad mRNAs and inhibition of host protein synthesis are shown to involve viral-mediated underphosphorylation of cap-binding protein (CBP) and subsequent inactivation of CBP complex, a large enzymatic complex required for cap-dependent mRNA translation. Late Ad mRNAs, like those of poliovirus, possess the unique ability to translate independent of a normal cap recognition process and do not require the activity of CBP complex. Inhibition of cellular translation by these two viruses is quite similar, except that whereas CBP complex is proteolytically degraded by poliovirus, it is functionally inactivated by Ad.
腺病毒（Ad）感染会导致细胞蛋白质合成在病毒感染周期后期开始时受到显著抑制。我们发现，Ad利用细胞周期进程中用于抑制细胞蛋白质合成的机制来抑制宿主并增强晚期病毒mRNA的翻译。细胞mRNA与晚期Ad mRNA之间的区分以及宿主蛋白质合成的抑制被证明涉及病毒介导的帽结合蛋白（CBP）的低磷酸化以及随后CBP复合物的失活，CBP复合物是帽依赖性mRNA翻译所需的一种大型酶复合物。晚期Ad mRNA与脊髓灰质炎病毒的mRNA一样，具有独立于正常帽识别过程进行翻译的独特能力，并且不需要CBP复合物的活性。这两种病毒对细胞翻译的抑制非常相似，只是脊髓灰质炎病毒会通过蛋白水解作用降解CBP复合物，而Ad则使其功能失活。
