人类角质细胞表现出有限的SARS-CoV-2感染潜力,尽管ACE2和成熟的cathepsin L表达
Leslie Hertereau1, Manon Barthe1,2, Noura Lamghari1
1Université Côte d'Azur, Centre National de la Recherche Scientifique (CNRS) UMR7275, Institut National de la Santé et de la Recherche médicale (INSERM) U1323, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Valbonne, France.
JID innovations : skin science from molecules to population health
|February 2, 2026
概括
严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 尖端蛋白在皮肤中发现,但病毒不能在皮肤细胞中复制. 然而,SARS-CoV-2可能会进入皮肤细胞,可能导致炎症.
科学领域:
- 病毒学 病毒学
- 皮肤病学 皮肤病学
- 细胞生物学 细胞生物学
背景情况:
- 在感染患者的皮肤中检测到严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 蛋白质.
- 对于SARS-CoV-2直接感染皮肤细胞的潜力仍然未被评估.
- SARS-CoV-2 进入细胞涉及ACE2受体和TMPRSS2介导的融合或甲素L-依赖性内细胞形成.
研究的目的:
- 评估SARS-CoV-2入口受体和核心受体在人类初级角质细胞和纤维细胞中的表达.
- 为了确定SARS-CoV-2是否可以感染这些皮肤细胞.
主要方法:
- 在角质细胞和纤维细胞中对ACE2,TMPRSS2,cathepsin L基因和蛋白质表达的定量评估.
- 在实验室感染测试使用SARS-CoV-2Delta变体对初级角质细胞进行.
主要成果:
- 人类角质细胞表达主要的SARS-CoV-2受体ACE2,在分化和TLR3激活过程中上调调节.
- 角质细胞缺乏融合核受体TMPRSS2,但表达成熟的甲素L.
- 在SARS-CoV-2的Delta变异结合状细胞的细胞表面,但不能在细胞内复制.
结论:
- 由于没有TMPRSS2.2,在角质细胞中活跃的SARS-CoV-2复制不太可能发生.
- 在角质细胞中ACE2的诱导上调可能允许有限的皮肤病毒进入,可能导致局部炎症和传播.
- 需要进一步的研究,以探索皮肤病毒进入的影响.
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