Influenza virus uses mGluR2 as an endocytic receptor to enter cells

文献类型： 外文期刊

第一作者： Ni, Zixin

作者： Ni, Zixin;Wang, Jinliang;Yu, Xiaofei;Wang, Yifan;Wang, Jingfei;He, Xijun;Li, Chengjun;Deng, Guohua;Shi, Jianzhong;Kong, Huihui;Jiang, Yongping;Chen, Pucheng;Zeng, Xianying;Tian, Guobin;Chen, Hualan;Bu, Zhigao

作者机构：

期刊名称：NATURE MICROBIOLOGY （ 影响因子：28.3； 五年影响因子：22.9 ）

ISSN： 2058-5276

年卷期： 2024 年

页码：

收录情况： SCI

摘要： Influenza virus infection is initiated by the attachment of the viral haemagglutinin (HA) protein to sialic acid receptors on the host cell surface. Most virus particles enter cells through clathrin-mediated endocytosis (CME). However, it is unclear how viral binding signals are transmitted through the plasma membrane triggering CME. Here we found that metabotropic glutamate receptor subtype 2 (mGluR2) and potassium calcium-activated channel subfamily M alpha 1 (KCa1.1) are involved in the initiation and completion of CME of influenza virus using an siRNA screen approach. Influenza virus HA directly interacted with mGluR2 and used it as an endocytic receptor to initiate CME. mGluR2 interacted and activated KCa1.1, leading to polymerization of F-actin, maturation of clathrin-coated pits and completion of the CME of influenza virus. Importantly, mGluR2-knockout mice were significantly more resistant to different influenza subtypes than the wild type. Therefore, blocking HA and mGluR2 interaction could be a promising host-directed antiviral strategy. Influenza virus uses metabotropic glutamate receptor 2 (mGluR2) as an endocytic receptor to enter cells through clathrin-mediated endocytosis.

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