人肝癌细胞感染蓝舌病毒HbC_3株超微结构的动态观察  

Dynamic Observation Microstructure of the Human Hepatic Carcinoma Cells Infected Bluetongue Virus HbC_3 Strain

作　　者：汪艳[1] 雷森林[2] 郭淑芳[1] 易有荣[1] 董长垣[1] 

机构地区：[1]武汉大学医学院病毒学国家重点实验室,430071 [2]武汉大学医学院结构生物学研究中心,430071

出　　处：《肿瘤防治研究》2006年第12期856-858,共3页Cancer Research on Prevention and Treatment

基　　金：国家自然科学基金资助项目(30271471)

摘　　要：目的 探讨蓝舌病毒靶向抗肿瘤的细胞生物学机制。方法 利用透射电镜观察蓝舌病毒HbC3株感染人肝癌细胞Hety-3B的形态发生学以及该病毒引起的细胞的病理改变。结果 BTV-HbC3以受体介导的胞饮作用穿入细胞，溶酶体水解病毒外衣壳，使之成为亚病毒粒子，胞浆内有病毒包涵体及未装配成熟的亚病毒颗粒。随后亚病毒颗粒装配上外层蛋白结构，形成成熟的病毒粒子。病毒感染细胞12～18h时，细胞以挤出的方式释放病毒并达到高峰。18-48h时，病毒进入超感染期，大量细胞发生病变，出现细胞凋亡和溶解。结论 一旦蓝舌病毒感染Hep-3B肿瘤细胞即可在细胞内增殖并诱导该肿瘤细胞进入凋亡，死亡的肿瘤细胞释放出的病毒粒子并再次感染其他肿瘤细胞，直至将全部肿瘤细胞杀灭，其溶瘤方式为链式反应。Objective The cytobiological mechanism of BTV-HbC3 killed the tumor cells were investigated in this study. Methods The morphogenesis and the pathological changes of the Hep-3B cells infected Bluetongue virus were studied by transmission electron microscope. Results BTV-HbC3 were penetrated into cell with pinocytpsis. Viral outside capsid were hydrolated with hydrolase in the lysosome, which become subvirual particles. The viral inclubodies and subviral particles without outer layer proteins were observed in the plasma. Many subviral particles have been assembled in outer layer proteins to become mature viral particles. In 12-18 hours infection, virus was released from the infected cells. In this case, the rate of releasing virus was increased rapidly up to a maximum. In 18-48 hours infection, virus entered into superinfection and pathological changes of many cells were found, and apoptosis and lyse were also observed on some of them. Conclusion As soon as BTV HbC3 infected tumor cells, it can selectively replicate in tumor cells and induce tumor cells into apoptosis. Viral particles were released from dead cells and infected other cells until all tumor cells were killed. The oncolytic ways of BTV-HbC3 was called chain reaction.

关 键 词：蓝舌病毒HbG(BTV-HbC3) 人肝癌细胞(Hep-3B) 形态发生学 溶癌病毒 

分 类 号：R730.231[医药卫生—肿瘤] R735.7[医药卫生—临床医学]