狂犬病是由狂犬病病毒（Rabies virus, RABV）引起的重要人兽共患病，其致死率几乎为100%，对公共卫生安全造成巨大威胁。病毒感染中枢神经系统后，神经细胞自噬在抗病毒免疫应答和保护神经细胞功能等方面发挥重要作用。前期研究表明：RABV感染后可诱导神经细胞发生Beclin 1相关的细胞自噬，且宿主自噬相关因子Bif-1（Bif-1可与Beclin 1相互作用促进自噬的发生）的表达存在显著差异，病毒感染细胞中Bif-1与LC3共定位表达，表明Bif-1参与了RABV诱导的神经细胞自噬。本研究拟在前期研究基础上揭示Bif-1与RABV感染诱导神经细胞自噬的相互关系，研究Bif-1介导神经细胞自噬对RABV致病性和宿主抗病毒免疫应答的影响，阐述Bif-1对神经细胞自噬的调控及其分子机制，为进一步研究RABV的感染特性和致病机制，筛选新型治疗药物和靶点奠定基础。

Rabies, caused by rabies virus (RABV), is a major zoonotic disease with a mortality rate of almost 100%, which remains an important public health problem in China. After central nervous system infected by virus, neuronal autophagy plays an important role in antiviral immune response and protection of neuron. Our previous studies showed that RABV infection could induce neuronal autophagy which was related to Beclin 1; the expression of the host autophagy related factor Bif-1 (Bif-1 interacted with Beclin 1 to promote autophagy) had significant differences after RABV infection; Bif-1 was found to co-localize with LC3 in infected cells. The results indicated that Bif-1 was involved in neuronal autophagy induced by RABV. Based on the early background research, this study will discuss the relationship between Bif-1 and neuronal autophagy induced by RABV and research Bif-1 mediated neuronal autophagy effect on the pathogenicity of RABV and host antiviral immune response. Moreover, the study wants to find the regulation and molecular mechanism of Bif-1 on neuronal autophagy. It provides the groundwork for further study of infection characteristics and pathogenic mechanism and development of new treatment drugs and targets.