miR-2459调控锌指抗病毒蛋白ZAP表达介导对BVDV复制水平的影响分子机制研究

牛病毒性腹泻病毒BVDV与宿主细胞相互作用的分子机制尚不清楚，直接限制了BVDV疫苗的研发与相关防治新技术的研究。因此，其相互作用的分子机制亟待阐明。本课题组前期研究发现BVDV NADL侵染MDBK细胞后显著性增加了miR-2459的表达，并通过生物信息学软件预测发现miR-2459靶向ZAP基因3’UTR 48-54 nt区域。众所周知，ZAP是一种天然免疫抗病毒效应因子，能抵御多种病毒（例如艾滋病病毒、乙肝病毒、埃博拉病毒等）的感染。所以，课题组拟在前期研究工作的基础上研究miR-2459靶向ZAP基因并调控其表达，进而影响BVDV的复制，并系统探究ZAP影响BVDV复制的分子机制，其结果将为阐述BVDV与宿主细胞之间的相互作用关系及研究有效抗BVDV的新技术和新策略提供坚实的理论依据。

The mechanisms of the interaction of bovine viral diarrhea virus（BVDV）and host cells remain unclear, and directly restrict the research and development of BVDV vaccine and prevention methods. In our previously study, we found that miR-2459 mRNA relative levels were significantly increased in BVDV NADL-infected MDBK cells. Prediction of the targets of miR-2459 using TargetScan shown that miR-2459 targeted the 3’UTR 48-54 nt miRNA recognized sites of Zinc finger antiviral protein (ZAP). ZAP is an innate immunity anti-viral effect factor and defenses the replication of several viruses, such as HIV、HBV and EBOV. Therefore, based on the previous research, we focus on the molecular mechanisms of miR-2459 targets ZAP and regulates its expression, and mediated inhibiting BVDV replication and the molecular mechanisms of ZAP inhibiting BVDV replication. The achievements of our research provide a stable theoretical basis for expounding the interactions of BVDV and host cells, and provide a new strategy and technology for anti-BVDV.