水貂阿留申病毒抗体依赖性感染增强作用的可能机制探讨  

Eenie,Meenie,Miney,Moe,Who Is Responsible for the Antibody-Dependent Enhancement of Aleutian Mink Disease Parvovirus Infection?

作　　者：朱洪伟[1] 邢秀梅[1] 温永俊[1] 

机构地区：[1]中国农业科学院特产研究所吉林省特种经济动物分子生物学-省部共建国家重点实验室培育基地,长春130112

出　　处：《病毒学报》2014年第4期450-455,共6页Chinese Journal of Virology

基　　金：吉林省科技发展计划项目"吉林省特种经济动物疫病防控研究创新团队"(项目编号:20121823)

摘　　要：水貂阿留申病毒(Aleutian mink disease parvovirus,AMDV)主要侵害宿主的单核-巨噬细胞,引起持续性感染。病毒感染后可产生免疫复合物疾病、高γ球蛋白血症和高水平的抗体,抗病毒抗体在体内不能有效地清除病毒,反而通过Fc受体介导的抗体依赖性感染增强作用(Antibody-dependent enhancement,ADE)使感染增强,并造成免疫系统功能紊乱。目前,ADE的可能感染致病机制为①抗体复合物与FcR受体、补体成分C3或C1q、C1qR结合,促进了病毒与细胞的吸附;②免疫复合物通过上调模式识别受体的负调控因子抑制了干扰素介导的抗病毒机制;③通过IL-10的早期活化,抑制机体的先天性免疫抗病毒机制。本文就AMDV ADE作用的几种可能机制以及ADE在致病过程中的作用进行了探讨,以期为ADE的分子机制研究、病毒的致病机理及疫苗设计提供参考。Aleutian mink disease parvovirus（AMDV）causes a persistent infection associated with immune complex disease,hypergammaglobulinemia,and high levels of antiviral antibodies.Despite the presence of an antibody,the virus is not cleared in vivo.Pre-existing antibodies may enhance viral infections,by Fcreceptor-mediated antibody-dependent enhancement（ADE）,but the mechanism that underlies ADE has not been fully defined.Three models have been proposed,including：①interactions between antibody and FcR,complement C3fragment and CR,or between C1q and C1qR,which promotes viral attachment to cells;②suppression of IFN-γ-mediated host-cell antiviral gene expression by the upregulation of negative regulators of pathogen pattern recognition;and③the promotion of early IL-10secretion.In addition,the role of cytokine IL-6in ADE mediated disease development is discussed,to facilitate a better understanding of the pathogenesis of AMDV infection,as well as give insights into rational vaccine design approaches.

关 键 词：水貂阿留申病毒 抗体依赖性感染增强 病毒-抗体复合物 FC受体 

分 类 号：S852.65[农业科学—基础兽医学]