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神经皮林-1 促进SARS-CoV-2 细胞进入和感染性

Ludovico Cantuti-Castelvetri^1,2, Ravi Ojha³, Liliana D Pedro^1,2

¹Institute of Neuronal Cell Biology, Technical University Munich, Munich, Germany.

Science (New York, N.Y.)

|October 21, 2020

概括

神经-1 (NRP1) 通过结合其裂部位显著增强严重急性呼吸综合征冠状病毒2 (SARS-CoV-2) 的传染性. 阻止NRP1或改变分裂部位可以减少病毒的进入,从而提供潜在的抗病毒策略.

科学领域:

病毒学
细胞生物学
免疫学

背景情况:

严重急性呼吸综合征冠状病毒2 (SARS-CoV-2) 是导致COVID-19的原因.
病毒组织热带性通常由宿主细胞表面受体和进入辅因子决定.
了解SARS-CoV-2的进入机制对于开发有效的干预措施至关重要.

研究的目的:

调查神经素-1 (NRP1) 在SARS-CoV-2细胞进入和感染性中的作用.
为了确定阻止SARS-CoV-2感染的潜在宿主目标.

主要方法:

评估了NRP1对SARS-CoV-2感染性的影响.
使用单克隆抗体阻止NRP1.
创建并测试了一种具有改变素分裂部位的SARS-CoV-2突变体.
对人类COVID-19尸检嗅觉上皮进行病理分析.

主要成果:

神经蛋白-1 (NRP1) 显著增强了SARS-CoV-2的感染力.
单克隆抗体对NRP1的阻断抑制了这种增强.
一种突变的SARS-CoV-2具有改变的素分裂部位,显示其对NRP1的依赖性减少.
发现SARS-CoV-2感染了人体嗅觉上皮的NRP1阳性细胞.

结论:

NRP1是增强SARS-CoV-2传染性的关键因素,特别是通过与病毒裂部位的相互作用.
嗅觉上皮质中的NRP1阳性细胞被SARS-CoV-2感染.
NRP1 是抗病毒治疗COVID-19的一个有希望的目标.

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