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ACE2独立的SARS-CoV-2病毒通过单细胞表面GRP78进入单细胞 - - 来自转化临床和实验方法的证据

Bing Han¹, Yibing Lv², Dominique Moser¹

¹Laboratory of Translational Research 'Stress and Immunity', Department of Anesthesiology, LMU Hospital, Ludwig-Maximilians-Universität in Munich, Munich, Germany.

|November 15, 2023

概括

严重的COVID-19涉及单细胞和巨细胞. 这项研究表明细胞表面GRP78 (csGRP78) 作为SARS-CoV-2受体,使ACE2独立的病毒进入这些关键免疫细胞.

科学领域:

病毒学和免疫学病毒学和免疫学
细胞生物学细胞生物学
传染性疾病传染性疾病

背景情况:

严重的COVID-19病原体涉及单细胞和巨细胞,但这些细胞表达低ACE2,已知的SARS-CoV-2入口受体.
建议使用SARS-CoV-2进入单细胞/巨细胞的替代机制,预测GRP78是潜在的受体.
GRP78在单细胞和巨细胞上具有构成性表达.

研究的目的:

研究细胞表面GRP78 (csGRP78) 作为单细胞和巨细胞中的SARS-CoV-2受体的作用.
为了探索ACE2独立的病毒进入COVID-19免疫细胞的途径.

主要方法:

与对照组相比,住院COVID-19患者的炎症状态和csGRP78表达的特征.
对CD14+单细胞的转录组分析和对支气管支气管洗液 (BALF) 数据集的生物信息再分析.
在体外验证SARS-CoV-2尖端蛋白和GRP78相互作用以及伪病毒吸收实验.

主要成果:

COVID-19患者在周围血液和肺单细胞/巨细胞上表现出典型的炎症,具有上调的csGRP78.
增加的促炎性细胞因子与增加的csGRP78表达相关.
SARS-CoV-2 尖端蛋白与 csGRP78 直接相互作用 (K_D = 55.2 nM),而高 GRP78 细胞显示伪病毒吸收增加.

结论:

细胞表面GRP78 (csGRP78) 作为SARS-CoV-2尖端蛋白的受体起作用.
csGRP78调解SARS-CoV-2的ACE2独立进入单细胞.
这突出了一个新的病毒进入机制,这对于了解COVID-19在特定免疫细胞群体中至关重要.

关键词:

细胞应激压力是细胞的压力.在 GRP78 中使用.单细胞 (Monocytes) 是一种单细胞.这就是SARS-CoV-2病毒.在THP-1细胞中.病毒的入口病毒的入口

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