miRNA在鸡体内对干扰素介导的抗病毒免疫应答的分子调控

项目名称： miRNA在鸡体内对干扰素介导的抗病毒免疫应答的分子调控

项目编号： No.31272537

项目类型： 面上项目

立项/批准年度： 2013

项目学科： 农业科学

项目作者： 王永山

作者单位： 江苏省农业科学院

项目金额： 81万元

中文摘要： miRNA是存在于细胞内的非编码小RNA，对宿主细胞和病毒的基因表达具有广泛的、性质各异的调节作用，在干扰素介导的抗病毒固有免疫应答中的调控中也是如此。本项目以传染性法氏囊病病毒（IBDV）强毒为模式病毒，以鸡为感染动物，探讨miRNA在鸡体内对干扰素介导的抗病毒免疫应答的分子调控。用Western blot和miRNA芯片，分析IBDV强毒感染的鸡B淋巴细胞与法氏囊组织中I型IFN诱导及其抗病毒信号转导通路中关键蛋白表达变化以及细胞miRNA表达差异，鉴定出显著影响I型IFN介导抗IBDV的关键蛋白基因表达的miRNA，分别在细胞和鸡体内进行特定miRNA过表达以及抑制表达实验，解析其在细胞和鸡体内对细胞IFN表达与释放的分子调控功能，发现并定位细胞抗IBDV复制的miRNA分子靶标。进一步认识病毒复制与宿主细胞抗病毒相互作用的分子免疫调控机制，为研制新型抗病毒药物与疫苗提供依据。

中文关键词： 传染性法氏囊病病毒（IBDV）；microRNA (miRNA)；抗病毒天然免疫；干扰素（IFN）；调控机理

英文摘要： MicroRNAs (miRNAs) are endogenous small noncoding RNAs that post-transcriptionally regulate gene expression by targeting specific messenger RNA (mRNA). miRNAs regulate many cellular processes including the interferon (IFN) mediated antiviral innate immune response by regulating pattern recognition receptor signaling. Infectious bursal disease virus (IBDV) causes severe immunosuppressive disease in young chickens. It continues to pose a significant threat to the poultry industry worldwide. Type I interferon(IFN) play an important role in antiviral immune responses by inhibiting IBDV replication in the cultural cells (in vitro), however, it has been reported that in vivo IBDV infection appeared to inhibit IFN responses. Its molecular regulation mechanism has not been clarified. To understand these questions, our current study will investigate the molecular mechanism of the cellular miRNA in the regulation of IFN mediated antiviral innate immune response by using the virulent strain of IBDV to infect chicken B-lymphocytes as well as the in vivo chicken as the infection models. The different expression of the key proteins are analyzed by Western blot and cellular miRNAs in the induction and antiviral signaling pathways of type 1 IFNs are determined by miRNA microarray in the IBDV infected chicken B-lymphocytes and b

英文关键词： infectious bursal disease virus (IBDV)；microRNA (miRNA)；antiviral innate immunity；interferon (IFN)；regulation mechanism