麻疹病毒N蛋白诱导细胞自噬及其分子机理研究

麻疹病毒（measles virus）是一类人和灵长动物的致病性的单负链RNA病毒，其感染可引起多种疾病，并引发系统性病理生理反应。全球每年有100万儿童死于麻疹，在我国，近几年的流行病学研究发现麻疹发病率有回升趋势。目前，麻疹病毒致病的作用机理及其与宿主细胞的相互关系有待深入，因此研究麻疹病毒感染引起的细胞学效应及其带来的病理后果具有重要意义。我们前期研究初步发现，麻疹病毒N蛋白可显著促进细胞发生自噬，表达麻疹病毒N蛋白的细胞在饥饿诱导条件下自噬显著增强，但N蛋白促进细胞自噬的分子机理及引起的生物学意义仍然不清楚，本研究将在现有工作基础上，深入研究麻疹病毒N蛋白诱导细胞自噬的功能，探索其作用机制和信号调控途径，解析麻疹病毒N蛋白诱导细胞自噬的活性位点，为更加全面地认识麻疹病毒感染引起的患者临床病理生理反应，理解麻疹病毒与宿主细胞和机体之间的关系，发展有效的治疗和预防手段提供理论依据。

Measles is still one of the most important infectious diseases in the world. Measles virus (MV) belongs to the morbillivirus genus of the paramyxovirus family, which contains a negative strand RNA genome packed in a ribonucleoprotein structure surrounded by transmembrane glycoproteins, the hemagglutinin (H protein), the fusion protein (F protein) and nucleoprotein (N protein) and other protein. Viral infection elicits a variety of host responses that enable the infected cells to induce autophage or apoptosis. In this project, we found that nucleoprotein of measles can prominently promote cancer cell autophagy, which activated autophagic associated gene (Atg) protein family members Atg-5 and Atg-7 activities respectively. However it is unclear currently that what is the function of autophagy-inducing effect of N protein. With the basis of our previous investigation, we will further our project on aspects about amino acid mutation for the molecular mechanism of N protein’s autophagic inducing effect on the cell. We confidently believe that our research results will contribute to the relationship between measles virus and its host cells, also the development and clinical treatment of measles virus.