宿主细胞磷酸激酶在新城疫病毒感染中的作用

THE ROLE OF PHOSPHOKINASE FROM HOST CELLS IN THE INFECTION THE OF NEWCASTLE DISEASE VIRUS

为探讨磷酸化通路在新城疫病毒（Newcastle disease virus,NDV）感染中的作用,使用多种蛋白磷酸激酶抑制剂和激活剂预处理细胞,比较处理后NDV在细胞上生长状况的差异。结果显示NDV在PKC蛋白激酶抑制剂处理的细胞上的生长受到抑制,这种抑制作用能够被PKC蛋白激酶激活剂中和,而PKA蛋白激酶抑制剂和p38MAPK蛋白激酶抑制剂对其影响不大。通过PKC蛋白激酶抑制剂的细胞毒性试验证实,这种抑制作用不是由于药物对细胞的毒性或者因药物加入而改变培养基pH值而造成的。病毒在staurosporine处理的细胞上的生长曲线试验显示,浓度在20~200 nmol/L能对病毒感染产生抑制作用,并且药物浓度越高,上清中病毒的滴度相对越低。本研究结果表明PKC磷酸化通路在新城疫病毒的感染过程中发挥了重要作用。

In order to explore cellular phosphorylation pathway involved in the Newcastle disease virus（NDV） infection,the effect of diverse activators and inhibitors to phosphokinase on NDV propagation were detected in this study.After treatment with activators or inhibitors to phosphokinase,DF1 were infected with Herts/33,a velogenic NDV strain.The titer of virus in the supernatant was determined every 8 hours.The propagation of NDV was inhibited when pretreated with inhibitor of proteinkinase C,staurosporine,while this effect of propagation delay can be blocked by activator of proteinkinase C.To confirm the role of proteinkinase C phosphorylation pathway in the NDV infection,a propagation rate of the virus in cells pretreated with staurosporine was figured out.The results suggested that the concentration of staurosporine that could inhibit virus infection was 20-200 nmol/L.With higher of inhibitor concentration,the more obvious propagation delay were observed.In conclusion,the proteinkinase C plays a key role in the NDV infection.