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纳米扫描揭示了肝硫酸盐集群作为SARS-CoV-2附着和进入的对接点

Sue Han¹, Xin Wang¹, Tiansheng Li²

¹National Institute of Neurological Disorders and Stroke, 35 Convent Dr., Bldg. 35, Bethesda, Maryland 20892, USA.

bioRxiv : the preprint server for biology

|September 18, 2025

概括

肝素硫酸盐 (HS) 集群,而不是ACE2,介于SARS-CoV-2的附着和细胞进入. 阻止HS与pixantrone结合抑制了Omicron JN.1感染,揭示了HS作为一个关键的抗COVID-19目标.

科学领域:

病毒学病毒学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

对于了解病毒病原体而言,SARS-CoV-2 (COVID-19) 进入机制至关重要.
大多数人认为 ангиотензин转化酶2 (ACE2) 是主要的SARS-CoV-2受体.
细胞表面分子在病毒附着和进入中的精确作用需要进一步阐明.

研究的目的:

调查肝素硫酸盐 (HS) 和ACE2在SARS-CoV-2附着和细胞进入中的特定作用.
阐明SARS-CoV-2与细胞表面分子相互作用的机制.
评估针对HS病毒相互作用的治疗潜力.

主要方法:

先进的光显微镜可可视化单个病毒和受体.
通过SARS-CoV-2对HS集群结合的定量分析.
使用HS结合剂pixantrone对SARS-CoV-2Omicron JN.1变种进行抑制试验.

主要成果:

SARS-CoV-2 通过 heparan 硫酸盐 (HS) 分子集群附着在细胞表面,而不是直接附着在 ACE2.
从血中显著突出的HS群体,作为病毒附着的对接点.
皮克桑特隆通过阻断HS结合,显著抑制了SARS-CoV-2 Omicron JN.1在人类呼吸道细胞中的附着和感染.

结论:

肝素硫酸盐 (HS) 集群,而不是ACE2,是SARS-CoV-2细胞附着和内细胞形成的主要媒介.
在HS相互作用的下游,ACE2的功能是促进病毒基因组表达.
向HS病毒相互作用是对抗SARS-CoV-2以及潜在的其他病毒的有希望的治疗策略.

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