猪繁殖与呼吸综合征病毒（PRRSV）能够引起白介素-10(IL-10)升高进而诱导机体的免疫抑制，本课题组前期试验表明该病毒核衣壳蛋白（N蛋白）能够引起IL-10升高，但N蛋白诱导宿主免疫抑制的分子机制至今尚不清楚。本项目拟通过研究JAK1-STAT3、P38和PI3K信号通路阐述N蛋白诱导宿主IL-10升高进而引起免疫抑制的分子机制；利用蛋白解析技术探索N蛋白中诱导宿主IL-10分泌的关键氨基酸位点，进行该位点的定点突变，揭示N蛋白诱导IL-10表达水平变化进而引起免疫抑制的分子机制。本研究对阐明PRRSV免疫抑制机制及新型疫苗的设计具有重要意义。

Porcine reproductive and respiratory syndrome virus (PRRSV) is able to cause increased interleukin-10 (IL-10) and immunosuppression, and its viral capsid protein (N protein) has been determined to cause increased IL-10 in our preliminary experiments, but the molecular mechanism of host immunosuppression induced by N protein remains unknown so far. In this study, we plan to detect JAK1-STAT3, P38 and PI3K signaling pathways to explain the molecular mechanism of increased IL-10 and immunosuppression induced by N protein. Then protein analytical techniques are applied to identify the key amino acid sites on N protein inducing host IL-10 secretion. The key amino acid sites are mutated to elucidate the molecular mechanism of immunosuppression induced by N protein. This study has important significance to expound PRRSV immunosuppressive mechanism and novel vaccine design.