流感病毒和冠状病毒的细胞表面结合与内化

鲍美美; 杨恺; 元冰

doi:10.7498/aps.69.20201161

摘要

病毒是一种在活细胞内寄生并以复制方式增殖的非细胞型生物. 不同病毒侵入细胞的方式不同, 但大都需要通过结合至细胞表面特定的受体蛋白或脂质结构来实现细胞内化, 从而启动入侵程序和感染宿主细胞. 因此揭示病毒结合和内化侵入细胞的具体过程及机制有助于从源头上开发靶向药物或疫苗. 本文以流感病毒和冠状病毒为例, 首先介绍了流感病毒的结构, 其与细胞膜上特定种类蛋白或脂质结构的结合方式, 其完成细胞内吞的途径及诱导其内化的细胞因子种类, 以及侵入细胞后的作用过程, 继而对冠状病毒尤其针对目前仍在全球范围内肆意传播的新型冠状病毒(SARS-CoV-2), 扼要阐述了其结构特点、与细胞受体血管紧张素转化酶ACE2的结合及实现细胞内化的研究进展.

关键词:

Abstract

Viruses are acellular organisms that must be parasitized in living cells and proliferated by replication. Although different viruses invade cells in different ways, they mainly initiate the invasion process through binding to specific receptor proteins or lipid structures on the cell surface for the following cellular internalization. Thus revealing the interaction process and underlying mechanism between viruses and cell membranes will be helpful in developing targeted drugs or vaccines from the source. In this review, the influenza virus and coronavirus are taken for example. We will first discuss the structure of influenza viruses, their binding modes with cell membranes, the way of realizing cell endocytosis and the cytokines involved in this process. After that, recent research progress of coronavirus especially the novel coronavirus SARS-CoV-2, including its structural characteristics, its binding with cell receptor ACE2 and the following cellular internalization, is briefly introduced.

Keywords:

作者及机构信息

苏州大学软凝聚态物理及交叉研究中心, 苏州　215006

通信作者: 杨恺, yangkai@suda.edu.cn ; 元冰, yuanbing@suda.edu.cn

基金项目: 国家自然科学基金 (批准号: 21422404, 21774092, U1532108, U1932121, 21728502)和江苏省自然科学基金 (批准号: BK20171207, BK20171210)资助的课题

Authors and contacts

Center for Soft Condensed Matter Physics and Intersectional Research, Soochow University, Suzhou 215006, China

Corresponding author: Yang Kai, yangkai@suda.edu.cn ; Yuan Bing, yuanbing@suda.edu.cn

Funds: Project supported by the National Natural Science Foundation of China (Grant Nos. 21422404, 21774092, U1532108, U1932121, 21728502) and the Natural Science Foundation of Jiangsu Province, China (Grant Nos. BK20171207, BK20171210)

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施引文献

图 1 流感病毒的结构与形状^[17,21]　(a) 丝状、杆状与球状流感病毒模型图, 流感病毒是包被病毒, 最外层是脂质膜, 膜上含有HA和NA两种糖蛋白及M2通道蛋白, 膜下是基质蛋白M1, 丝状病毒的基因组位于远端, 球状病毒的基因组位于中心; (b) 丝状病毒和(c) 球状病毒的电子显微镜照片

Fig. 1. Composition and shape of influenza virus^[17,21]: (a) Filamentous, rod-shaped and globular influenza virus models; (b), (c) representative electron microscopy images of filamentous and globular viruses, respectively.

下载: 全尺寸图片幻灯片

图 2 流感病毒在细胞表面结合及内化示意图. 流感病毒与细胞表面的糖蛋白或糖脂末端的唾液酸、或者磷酸化的糖蛋白、抑或是C型凝集素Langerin发生结合, 之后在G蛋白偶联受体FFAR2、表达于膜上的核仁蛋白、适配体蛋白Epsin1和EPS15、C型凝集素Langerin等细胞因子的参与下, 通过网格蛋白介导的方式发生内吞. 胞内Ca²⁺的增加可以促进流感病毒通过网格蛋白或非网格蛋白的方式侵入细胞, 另外膜上脂筏结构也参与病毒的吸附和内化过程

Fig. 2. Schematic diagram of influenza virus binding and internalization at cellular surface. The influenza virus binds on the cell surface with sialic acid at the end of a glycoprotein or lipid, phosphorylated glycoprotein, or C-type lectin Langerin, and then enters into the cell through clathrin-mediated endocytosis with the participation of cytokines such as G protein coupled receptor FFAR2, nucleolus protein expressed in membrane, adapter proteins Epsin1 and EPS15, or C-type lectin Langerin. An increased amount of intracellular Ca²⁺ promotes the entry of influenza virus in the clathrin or non-clathrin way. Lipid rafts also play roles in the process of virus adsorption and internalization.

下载: 全尺寸图片幻灯片

图 3 SARS-CoV-2的病毒结构^[80]及透射电子显微镜图像^[82]　(a) SARS-CoV-2的结构示意图; (b), (c) SARS-CoV-2在不同放大倍数下的透射电子显微镜图像

Fig. 3. Structure^[80] and transmission electron microscopy images^[82] of SARS-CoV-2: (a) Structure of SARS-CoV-2; (b), (c) visualization of SARS-CoV-2 under transmission electron microscope.

下载: 全尺寸图片幻灯片

表 1 流感病毒与宿主细胞结合的靶向分子

Table 1. Targeting molecules for influenza virus binding to host cells.

流感病毒作用点	宿主细胞结合点	阶段	文献
HA	唾液酸	结合	[23]
HA	磷酸化的糖蛋白	结合	[31]
HA	凝集素	结合	[32]

下载: 导出CSV

表 2 参与流感病毒内化的细胞因子

Table 2. Cytokines involved in influenza virus internali-zation.

细胞因子	阶段	功能
N-连接的糖蛋白	内化	可能存在病毒侵入细胞必要的特定碳水化合物构象^[72]
AP2 B1	内化	与FFAR2, β-arrestin1 形成信号级联反应^[54]
Epsin 1	内化	聚集网格蛋白, 启动形成CCPs^[55]
核仁蛋白	内化	与HA直接结合帮助病毒侵入细胞^[59]
C型凝集素	内化	骨髓的内吞受体, 将病毒转至早期内吞体^[32]
Ca²⁺	内化	激活PIP5 K-PLC信号通路调节CME和CIE路径^[68]
脂筏	内化	提供信号平台激活EGFR信号通路^[30]

下载: 导出CSV

map

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