MINK1是生发中心家族激酶成员，参与细胞生长、凋亡、细胞骨架重排及基因转录等多个细胞生命过程。近期研究表明，MINK1能通过调节人EV71病毒蛋白翻译参与病毒的复制，但其具体作用机制和在其它病毒感染过程中的调控作用尚不明确。我们前期的研究表明，MINK1缺失能抑制VSV在小鼠体内及细胞内的复制，提示MINK1在不同的病毒感染过程中起到广泛调节作用。基于MINK1在细胞内的已知生物学功能以及宿主细胞对病毒感染的反应，我们推测MINK1可能通过如下途径影响病毒复制：1、病毒的侵入及释放；2、病毒与宿主细胞互作；3、宿主细胞的抗病毒固有免疫反应。本课题拟采用实验室已有的MINK1基因敲除小鼠及其来源的细胞，就上述可能性进行研究，最终确定MINK1在病毒复制中的作用，阐明MINK1影响病毒复制的分子机制，从而为研发新的抗病毒药物和治疗策略提供理论依据。

MINK1 (Misshapen/NIK-related kinase 1) is a member of the germinal center family of kinases and regulates a wide variety of cellular processes, including cell growth, apoptosis, cytoskeletal rearrangement and gene transcription. Recently, it was proved that MINK1 also plays a role in the of replication of human EV71 (enterovirus 71) through the regulation of viral protein translation. However, many questions need to be solved when it comes to the role of MINK1 in viral protein translation and replication of other viruses. Our results show that MINK1 deficiency inhibits the replication of VSV (vesicular stomatitis virus) in mice and cells which indicates that MINK1 plays a role in the regulations of infection of various kinds of viruses. Based on the known functions of MINK1 in cell and the responses of cell to viral infection, we speculate that MINK1 may affect virus replication through the following ways: entry and release of virus; interactions between virus and host; the antiviral innate immune responses of host. So we decide to study these hypotheses using MINK1-/- mice and their cells to ascertain the functions of MINK1 in virus replication and the detailed molecular mechanisms. This study may provide us a new insight into the development of antiviral strategies or drugs.