汉滩病毒（HTNV）引起肾综合征出血热在我国发病人数多、病死率高，尚无有效治疗方法。HTNV感染直接损伤靶细胞是重要的致病机制，其如何逃逸干扰素抑制作用是备受关注的科学问题。文献和我们的研究表明，在HTNV感染后期重要干扰素刺激基因MxA和IFITM3表达受到抑制，而对应的miRNA-17和miRNA-29a明显升高。我们推测HTNV可能通过一定机制调控miRNA及ISG的表达，从而逃逸干扰素的抑制作用。进一步实验发现DDX17结合序列RCAYCH在miRNA-17和miRNA-29a前体也存在，且敲减DDX17上调MxA和IFITM3的表达；DDX17与NP共定位于细胞质。本项目拟明确HTNV感染时 NP与DDX17存在相互作用，并可调控miRNA-17和miRNA-29a的表达，并抑制MxA和IFITM3产生的机制，为理解HTNV感染后期IFN无法控制病毒复制的机理提供实验依据。

Hemorrhagic fever with renal syndrome caused by Hantaan virus (HTNV) has a large number of cases and a high mortality rate in our country and has no effective treatment method. The direct damage of target cells caused by HTNV infection is an important pathogenic mechanism, and how to escape the inhibitory effect of interferon is a scientific issue that has attracted much attention. According to literature and our research, the expression of important interferon-stimulating genes MxA and IFITM3 are suppressed in the late stage of HTNV infection, while the corresponding miRNA-17 and miRNA-29a are significantly increased. We speculate that HTNV may regulate the expression of miRNA and ISG through a certain mechanism, thereby escaping the inhibitory effect of interferon. Further experiments found that the DDX17 binding sequence RCAYCH was also present in the precursors of miRNA-17 and miRNA-29a, and knockdown of DDX17 up-regulated the expression of MxA and IFITM3; DDX17 and NP were co-localized in the cytoplasm. This project intends to clarify the interaction between NP and DDX17 during HTNV infection, which can regulate the expression of miRNA-17 and miRNA-29a to inhibit the production of MxA and IFITM3. It will provide experimental basis for understanding the mechanism by which IFN can not control virus replication in the later stage of HTNV infection.