项目名称: 石斑鱼肿瘤坏死因子受体相关因子6(TRAF6)在抗病毒天然免疫反应中的作用
项目编号: No.31202022
项目类型: 青年科学基金项目
立项/批准年度: 2013
项目学科: 畜牧学与草地科学、兽医学、水产学
项目作者: 魏京广
作者单位: 中国科学院南海海洋研究所
项目金额: 25万元
中文摘要: 石斑鱼是我国南方重要的海水名贵养殖鱼类之一,经济价值极高。在高密度集约化养殖条件下各种病害频繁爆发是其可持续健康发展的主要瓶颈,虹彩病毒SGIV是其中最严重的传染性病毒病原之一。目前,有关石斑鱼对SGIV感染的免疫应答机理仍不十分清楚。我们前期的研究表明,石斑鱼感染SGIV后,其先天性免疫因子TLR9、MyD88及IRF7在TLRs介导的抗病毒免疫反应诱导I型干扰素产生中发挥重要作用,而TRAF6 是该途径的重要信号转导分子。目前还没有鱼类TRAF6对病毒感染和复制的调节作用以及在抗病毒天然免疫反应中的作用机制报道。本项目拟在前期研究基础上,进一步克隆和表达石斑鱼TRAF6基因,系统研究TRAF6对SGIV感染和复制的调节作用以及在抗病毒天然免疫反应中的作用机制。研究成果将为阐明SGIV 感染和致病的分子机理奠定基础,为石斑鱼虹彩病毒病的预防和治疗提供新的理论依据和潜在靶点。
中文关键词: 石斑鱼;肿瘤坏死因子受体相关因子 6;新加坡石斑鱼虹彩病毒;抗病毒天然免疫反应;细胞凋亡
英文摘要: Grouper, Epinephelus spp., one of the major species being maricultured in China, are high-priced and popular seafood fish.However, with the rapid production and development of fish worldwide, fish diseases have become severe and threaten the fish industry in recent years. Singapore grouper iridovirus (SGIV) is a major viral pathogen causing high mortality and huge economic losses in grouper cultures. So far, the recognition mechanisms of host cells to SGIV infection remain poorly understood. Our previous studies indicated that grouper TLR9, MyD88 and IRF7 are potentially involved in type I IFNs production induced by TLRs-mediated antiviral immune responses to the invasion of SGIV, and play important roles in host innate defense against SGIV infection. TNF receptor-associated factor 6 (TRAF6) is an important signaling adapter molecule among the signaling.Now the roles of TRAF6 from fish in the regulation of viral infection and replication and the molecular mechanisms of host cells to antivial immune responses have not been reported. In this study, a new TRAF6 from orange-spotted grouper, Epinephelus coioides will be isolated and characterized on the basis of our previous research. The regulation of SGIV infection and replication and the molecular mechanisms of grouper cells to antiviral innate immune responses o
英文关键词: Epinephelus coioides;TNF receptorassociated factor 6 (TRAF6);Singapore grouper iridovirus (SGIV);antiviral innate immune responses;cell apoptosis