Receptors for enterovirus 71.
Receptors for enterovirus 71.
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DOI：
10.1038/emi.2014.49
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发表时间：
2014-07
影响因子：
13.2
通讯作者：
Koike, Satoshi
中科院分区：
文献类型：
--
作者：
Yamayoshi, Seiya;Fujii, Ken;Koike, Satoshi
肠道病毒71型(EV71)是手足口病的主要病原体之一。有时，EV71型感染与严重的神经系统疾病有关，如急性脑炎、急性迟缓性瘫痪和心肺衰竭。几个分子作为刺激EV71感染的细胞表面受体，包括清道夫受体B2(SCARB2)、P-选择素糖蛋白配体-1(PSGL-1)、唾液酸聚糖、硫酸乙酰肝素和膜联蛋白II(Anx2)。SCARB2在EV71的附着、病毒进入和脱壳过程中起着关键作用，它可以促进EV71的有效感染。已阐明了EV71成熟病毒粒子、前衣壳和空衣壳的三维结构，以及SCARB2的表面结构域。这些结构信息大大增加了我们对EV71感染早期步骤的了解。此外，SCARB2在体内EV71神经系统疾病的发生发展中起重要作用。成年小鼠不容易感染EV71，但表达人类SCARB2的转基因小鼠变得容易感染EV71，并患上与人类相似的神经系统疾病。这种小鼠模型有助于体内研究与EV71相关的许多问题。PSGL-1、唾液酸聚糖、硫酸乙酰肝素和Anx2是附着受体，通过将病毒滞留在细胞表面来增强病毒感染。这些分子还通过与SCARB2相互作用或独立于SCARB2，在体外促进病毒感染。然而，这些受体的协同作用，以及它们在体内对EV71致病作用的贡献，仍有待阐明。
Enterovirus 71 (EV71) is one of the major causative agents of hand, foot and mouth disease (HFMD). Occasionally, EV71 infection is associated with severe neurological diseases, such as acute encephalitis, acute flaccid paralysis and cardiopulmonary failure. Several molecules act as cell surface receptors that stimulate EV71 infection, including scavenger receptor B2 (SCARB2), P-selectin glycoprotein ligand-1 (PSGL-1), sialylated glycan, heparan sulfate and annexin II (Anx2). SCARB2 plays critical roles in attachment, viral entry and uncoating, and it can facilitate efficient EV71 infection. The three-dimensional structures of the mature EV71 virion, procapsid and empty capsid, as well as the exofacial domain of SCARB2, have been elucidated. This structural information has greatly increased our understanding of the early steps of EV71 infection. Furthermore, SCARB2 plays essential roles in the development of EV71 neurological disease in vivo. Adult mice are not susceptible to infection by EV71, but transgenic mice that express human SCARB2 become susceptible to EV71 infection and develop similar neurological diseases to those found in humans. This mouse model facilitates the in vivo investigation of many issues related to EV71. PSGL-1, sialylated glycan, heparan sulfate and Anx2 are attachment receptors, which enhance viral infection by retaining the virus on the cell surface. These molecules also contribute to viral infection in vitro either by interacting with SCARB2 or independently of SCARB2. However, the cooperative effects of these receptors, and their contribution to EV71 pathogenicity in vivo, remain to be elucidated.
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