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Bingting Ma¹, Cuiqing Huang^2,3, Jun Ma²

¹Beijing Advanced Innovation Center for Structural Biology, Beijing Frontier Research Center for Biological Structure, Center for Infectious Disease Research, Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing, P. R. China.

|October 14, 2021

概括

委内瑞拉马脑炎病毒 (VEEV) 的进入是由LDLRAD3介导的. 结构分析显示了VEEV-LDLRAD3相互作用,为开发VEEV进入抑制剂提供了基础.

科学领域:

结构生物学
病毒学
分子生物学

背景情况:

委内瑞拉马脑炎病毒 (VEEV) 在人类和马匹中引起严重的脑炎.
目前没有针对VEEV感染的疫苗或治疗方法.
低密度脂蛋白受体A类含域3 (LDLRAD3) 是一种新发现的VEEV宿主细胞受体.

研究的目的:

确定与VEEV复合的LDLRAD3域1 (LDLRAD3-D1) 的冷电子显微镜结构.
为了阐明LDLRAD3和VEEV之间的分子相互作用.
为了确定VEEV进入抑制剂的潜在目标.

主要方法:

低温电子显微镜 (cryo-EM) 用于确定高分辨率的结构.
结构分析以确定绑定接口和相互作用.
针对位点的突变发生,以调查关键的残留物和结合性亲缘关系.

主要成果:

确定了LDLRAD3-D1与VEEV病毒样粒子结合的3.0 Å冷-EM结构.
透露了LDLRAD3-D1的软木结构与VEEV E2-E1异构体通过疏水和极性接触相互作用.
确定了对VEEV结合至关重要的特定LDLRAD3- D1残留物;一些突变物表现出增强的结合亲和力.

结论:

该结构为VEEV-LDLRAD3相互作用提供了原子层面的洞察力.
LDLRAD3-D1 作为开发 VEEV 进入抑制剂的潜在支架.
这些发现有助于更好地了解阿尔法病毒的组合和受体结合,指导治疗的发展.

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