ICAM-1受体和感冒病毒

Jordi Bella , Michael G Rossmann
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引用次数: 52

摘要

人类鼻病毒(hrv)是普通感冒最重要的病原,是一种由二十面体蛋白外壳组成的小病毒,它包裹着一条单阳性RNA链。hrv的增殖发生在宿主细胞的细胞质中。为了产生感染,hrv必须首先附着在嵌入质膜的特定细胞受体上。90%的hrv免疫原性变异使用细胞间粘附分子-1 (ICAM-1)作为受体,ICAM-1是一种细胞表面糖蛋白,在炎症反应过程中促进细胞间信号传导。作为HRV受体,ICAM-1将病毒定位在膜的攻击距离内,然后触发病毒的构象变化,最终导致病毒RNA基因组通过脂质双分子层进入细胞质。通过结合hrv和ICAM-1片段的晶体结构以及配合物的电镜重建,分析了ICAM-1与hrv的相互作用。由此产生的分子模型有助于解决受体识别、结合特异性和ICAM-1诱导病毒脱壳的机制等问题。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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ICAM-1 receptors and cold viruses

Human rhinoviruses (HRVs), the single most important etiologic agent of common colds, are small viruses composed of an icosahedral protein shell that encapsidates a single, positive RNA strand. Multiplication of HRVs occurs in the cytoplasm of the host cell. To produce infection, HRVs must first attach to specific cellular receptors embedded in the plasma membrane. Ninety percent of HRVs immunogenic variants use as receptor intercellular adhesion molecule-1 (ICAM-1), a cell surface glycoprotein that promotes intercellular signaling in processes derived from inflammation response. As HRV receptor, ICAM-1 positions the virus to within striking distance of the membrane, and then triggers a conformational change in the virus that ultimately results in delivery of the viral RNA genome into the cytoplasm, across a lipid bilayer. The interaction between ICAM-1 and HRVs has been analyzed by the combination of crystal structures of HRVs and ICAM-1 fragments with electron microscopy reconstructions of the complexes. The resulting molecular models are useful to address questions about receptor recognition, binding specificity, and mechanisms by which ICAM-1 induces virus uncoating.

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