由汉滩病毒（HTNV）引起的肾综合征出血热在我国流行范围广，发病人数多，迄今缺乏特异有效的治疗药物。理解病毒复制周期有助于抗病毒药物靶点的发现，而在HTNV复制机制方面尚有许多不明之处。子代病毒的释放是HTNV复制的关键环节，已知其需要劫持并利用宿主蛋白转运系统，但具体作用机制不清楚。课题组前期发现HTNV包膜糖蛋白Gn胞质尾区存在类似逆转录病毒调控其释放的晚期结构域，且Gn可通过该结构域与宿主细胞的内吞体分选转运复合体（ESCRT）中的关键分子ALIX相互作用。故我们推测ALIX是衔接HTNV包膜糖蛋白和宿主细胞ESCRT，促进子代病毒释放的关键分子。为此，本项目拟研究HTNV通过Gn晚期结构域劫持宿主物质转运系统促进子代病毒释放的具体机制，同时探索靶向病毒释放筛选抑制药物干预HTNV复制的新策略。本研究将有助于理解汉坦病毒出胞的机制，并可为特异性抗病毒药物的研究提供新靶点。

Hemorrhagic Fever with Renal Syndrome (HFRS) caused by Hantaan Virus (HTNV) is a widespread disease in China, with a large number of cases and serious symptoms. At present, there is still a lack of specific and effective therapeutic drugs for HFRS, which seriously affects the control of HTNV infection. The research for antiviral drugs needs a thorough understanding of virus replication cycle, but there are still unknown aspects about HTNV, especially the release of progeny viruses. It is known that the release of HTNV is closely related to its glycoprotein, but the underlying mechanism is unclear. Our research shows that there is a conservative motif locates in the cytoplasmic tail of HTNV glycoprotein Gn, similar to retrovirus Gag protein which regulates virus budding. Also we find that Gn interact with ALIX, a key molecule in the host endosomal sorting complex required for transport (ESCRT), which is responsible for protein transport in host cells. Therefore, we speculate that ALIX is a key molecule to link HTNV glycoprotein with host cell ESCRT and promote budding of progeny viruses. Therefore, we intend to study the mechanism of how HTNV facilitate the release of progeny virus via its late domain by hijacking host protein transport system, and to explore targeted intervention methods against HTNV budding. This research will clarify the budding mechanism of HTNV progeny virus and provide new targets for the research of antiviral drugs.