Giron M, Logeat F, Fossar N, Huppert J
J Gen Virol. 1978 Sep;40(3):577-85. doi: 10.1099/0022-1317-40-3-577.
Poly (A) polymerase activity has been measured in crude cytoplasmic extracts of mouse L cells infected with encephalomyocarditis (EMC) virus. After infection there is first a decrease in enzyme activity followed by an increase which itself precedes detectable virus RNA and protein synthesis. The activity of the enzyme then declines before the release of mature virions and cell death take place. The early inhibition of poly (A) polymerase activity is correlated with the virus-induced shut-off of cellular protein synthesis but it is not due to inhibition of the synthesis of cellular enzyme and occurs in the absence of virus replication. The poly (A) polymerase is not synthesized after infection and modification of its activity can be reversed late in the virus cycle. These results indicate that host poly (A) polymerase activity can be regulated by the virus and further show that there is a correlation between the modification of poly (A) polymerase activity and the biosynthesis of poly (A).
已对感染脑心肌炎(EMC)病毒的小鼠L细胞的粗制细胞质提取物中的聚(A)聚合酶活性进行了测定。感染后,酶活性首先下降,随后升高,而这种升高先于可检测到的病毒RNA和蛋白质合成。然后,在成熟病毒粒子释放和细胞死亡发生之前,该酶的活性下降。聚(A)聚合酶活性的早期抑制与病毒诱导的细胞蛋白质合成关闭有关,但这不是由于细胞酶合成的抑制,并且在没有病毒复制的情况下也会发生。感染后聚(A)聚合酶不会合成,其活性的改变在病毒周期后期可以逆转。这些结果表明宿主聚(A)聚合酶活性可受病毒调节,并且进一步表明聚(A)聚合酶活性的改变与聚(A)的生物合成之间存在相关性。