Burdick J R, Durand D P
Antimicrob Agents Chemother. 1974 Oct;6(4):460-4. doi: 10.1128/AAC.6.4.460.
The response of Newcastle disease virus replication to primaquine, an antimalarial drug, was examined in chicken embryo cells (CEC). Virus-induced hemadsorption was completely inhibited by 250 mug of primaquine per ml. At lower concentrations, hemadsorption inhibition was dose dependent. Primaquine retarded virus-induced redistribution of receptor sites on the host cell plasma membrane as shown by the failure of infected, drug-treated CEC to be agglutinated with concanavalin A. The production of infectious progeny virus was substantially inhibited by the addition of primaquine at various times postinfection. When the drug was added early in the virus replication cycle, viral ribonucleic acid (RNA) synthesis was inhibited; however, when the drug was added late in the cycle, stimulation of RNA synthesis was observed. Primaquine was also shown to retard the incorporation of [(14)C]amino acids into proteins of virus-infected CEC. We suggest that the major role of primaquine is inhibition of protein synthesis; this results in changes in: hemadsorption, redistribution of lectin receptors, release of progeny, and virus-induced RNA synthesis.
在鸡胚细胞(CEC)中检测了抗疟药伯氨喹对新城疫病毒复制的反应。每毫升250微克的伯氨喹可完全抑制病毒诱导的血细胞吸附。在较低浓度下,血细胞吸附抑制呈剂量依赖性。如用刀豆球蛋白A处理感染药物的CEC未能发生凝集所示,伯氨喹可延缓病毒诱导的宿主细胞质膜上受体位点的重新分布。在感染后的不同时间添加伯氨喹可显著抑制感染性子代病毒的产生。当在病毒复制周期早期添加药物时,病毒核糖核酸(RNA)合成受到抑制;然而,当在周期后期添加药物时,则观察到RNA合成受到刺激。伯氨喹还被证明可延缓[(14)C]氨基酸掺入病毒感染的CEC的蛋白质中。我们认为伯氨喹的主要作用是抑制蛋白质合成;这导致了血细胞吸附、凝集素受体重新分布、子代释放以及病毒诱导的RNA合成的变化。