随着SARS-CoV-2的进化,增强了内细胞吸收,同时保持了TMPRSS2-依赖的融合
Clara L Magnus1, Zeliha Hamed Jaber1, Andreas Hiergeist2
1Institute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
Frontiers in immunology
|January 28, 2026
概括
在SARS-CoV-2的Omicron变种中,细胞进入的目的不仅仅是直接融合,而是利用内细胞结合,从而增强上呼吸道的复制和传播能力. 然而,它们保留了融合活性,保持了下呼吸道感染的潜力,对一些人来说构成风险.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 传染性疾病 传染性疾病
背景情况:
- 一种令人担忧的SARS-CoV-2变种Omicron表现出增加的传染性和感染性,但降低了病原性.
- 这种病毒性转变与病毒进入机制的改变有关,有利于内细胞形成而不是直接融合.
研究的目的:
- 为了比较各种SARS-CoV-2变体的进入机制 (内细胞分裂与直接融合),包括Omicron.
- 研究特定突变在确定病毒进入途径中的作用.
主要方法:
- 在四个人类细胞系中分析了九种临床SARS-CoV-2分离物 (野生型,阿尔法,三角形,欧米克朗).
- 使用TMPRSS2抑制剂 (卡莫斯塔特) 和甲素抑制剂 (阿洛克西斯塔丁) 来区分进入途径.
- 通过下一代测序确定全长的病毒基因组.
主要成果:
- 阿尔法和三角形变体主要使用TMPRSS2-依赖的融合.
- 奥米克朗变体显示出明显的转向内细胞分裂,特别是在特定的细胞类型中.
- 某些突变 (Δ69/Δ70,L452R,F486V) 与对内细胞吸收的依赖性增加有关.
结论:
- 奥米克龙变体通过保持融合活性,同时增强内细胞分裂,扩大了它们的细胞热带.
- 观察到上呼吸道复制和传播能力增加,但下呼吸道感染能力保持不变.
- 特定的突变组合可能会赋予选择性优势,有助于它们的流行.
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