Mahy B W, Siddell S, Wege H, ter Meulen V
J Gen Virol. 1983 Jan;64 (Pt 1):103-11. doi: 10.1099/0022-1317-64-1-103.
The multiplication of murine coronavirus strains A59 or JHM in Sac(-) cells was unaffected by the presence of alpha-amanitin at concentrations which inhibited the host cell DNA-dependent RNA polymerase activity. In cells infected with the A59 virus strain, actinomycin D-resistant RNA synthesis could readily be detected by pulse-labelling with [3H]uridine; this virus-specific RNA synthesis was not induced in the presence of the protein synthesis inhibitor anisomycin. A new RNA-dependent RNA polymerase activity was detected in the large particle fraction of A59 virus-infected cells. Optimal conditions for enzyme activity in vitro were established. Maximum activity occurred 5 h after infection, coincident with the peak of virus-specific RNA synthesis detected by pulse-labelling in vivo.
鼠冠状病毒株A59或JHM在Sac(-)细胞中的增殖不受α-鹅膏蕈碱存在的影响，该浓度的α-鹅膏蕈碱可抑制宿主细胞DNA依赖性RNA聚合酶活性。在用A59病毒株感染的细胞中，通过用[3H]尿苷脉冲标记可以很容易地检测到放线菌素D抗性RNA合成；在蛋白质合成抑制剂茴香霉素存在的情况下，这种病毒特异性RNA合成不会被诱导。在A59病毒感染细胞的大颗粒部分中检测到一种新的RNA依赖性RNA聚合酶活性。确定了体外酶活性的最佳条件。感染后5小时出现最大活性，这与体内脉冲标记检测到的病毒特异性RNA合成峰值一致。
