病毒性出血性败血症（VHS）是由病毒性出血性败血症病毒（VHSV）引起的严重危害多种海淡水养殖鱼类的传染性疾病。目前对于VHSV尚无有效的治疗方法，其致病机理研究也十分有限。免疫逃逸是病毒感染的重要致病机制，其中抑制宿主抗原呈递是病毒免疫逃逸的一种重要策略。在前期研究中发现，海鲈IFN-γ可通过STAT1-IRF1-CIITA信号轴诱导MHCII表达，而VHSV感染可抑制IFN-γ对MHCII的诱导，且该过程中核蛋白N发挥主要功能。本项目拟在此基础上，通过双荧光素酶报告基因实验、免疫共沉淀以及GST-pull down等方法，深入分析VHSV核蛋白N影响海鲈MHCII表达的分子机制。本研究将为阐明VHSV免疫逃逸机制奠定理论基础，同时为VHSV减毒疫苗的设计和抗病毒药物的开发提供潜在靶点。

Viral hemorrhagic septicaemia (VHS) is an infectious disease caused by viral hemorrhagic septicaemia virus (VHSV), which is harmful to a variety of marine and freshwater fish. Currently, there is no effective treatment for VHSV, and the research on its pathogenesis is very limited. Immune escape is an important pathogenic mechanism of viral infection, and inhibition of host antigen presentation is an important strategy for viral immune evasion. In previous studies, it was found that sea bass IFN-γ could induce the expression of MHCII through the STAT1-IRF1-CIITA signal axis, while VHSV infection could inhibit the induction of MHCII by IFN-γ, and nuclear protein N played a major role in this process. Based on previous studies, this project will take experimental measures including luciferase reporter gene assay, co-immunoprecipitation and GST-pull down to deeply analyze the molecular mechanism of MHCII expression suppressed by VHSV nuclear protein N. This study will lay the theoretical foundation for elucidating the immune escape mechanism of VHSV and provide potential target for the design of attenuated VHSV vaccine and the development of antiviral drugs.