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在旁观者细胞中,SARS-CoV-2感染会诱导ZBP1依赖的PANoptosis

Bo Yang^1,2, Ao Hu^1,2, Tiantian Wang^1,2

¹Institute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, Guangdong, China.

Proceedings of the National Academy of Sciences of the United States of America

|July 8, 2025

概括

严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 感染引发旁观者细胞中的PANoptosis,延长炎症和组织损伤. 抑制这种途径可以治疗COVID-19和其他病毒性疾病.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
细胞生物学细胞生物学

背景情况:

过度的炎症导致病毒性呼吸道感染的病理.
病毒感染,炎症和组织损伤之间的联系机制尚不清楚.
严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 作为研究这些过程的模型.

研究的目的:

阐明SARS-CoV-2感染引发持续炎症和组织损伤的机制.
在病毒感染期间研究PANoptosis在旁观者细胞中的作用.
确定潜在的治疗点,以减轻病毒引起的病理.

主要方法:

研究的SARS-CoV-2感染模型.
分析了循环GMP-AMP合成酶 (cGAS) 刺激干扰素基因 (STING) 途径的激活.
检查了STING诱导的自中介ADAR1降解和Z核酸积累.
在旁观者细胞中研究了ZBP1依赖的PANoptosis.
利用SARS-CoV-2和流感A病毒感染的小鼠模型.
评估了cGAS通路抑制和STING淘汰的作用.

主要成果:

在旁观者细胞中,SARS-CoV-2感染会诱导PANoptosis.
感染细胞中cGAS-STING通路的激活导致炎症介质的分泌.
这些介质触发了STING诱导的自中介ADAR1降解,导致Z-核酸积累.
在旁观者细胞中,Z-核酸的积累激活了ZBP1依赖的PANoptosis.
在小鼠模型中,抑制cGAS或STING淘汰会减少PANoptosis并减轻病理.

结论:

旁观者细胞中的PANoptosis是导致SARS-CoV-2感染病理损伤和持续炎症的关键机制.
在cGAS-STING-ADAR1-ZBP1轴中介于病毒诱导的旁观者细胞PANoptosis.
准旁观者细胞PANoptosis为COVID-19和其他病毒感染提供了潜在的治疗策略.

关键词:

这就是PANoptosis.这就是SARS-CoV-2病毒.在Z-核酸中.旁观者细胞旁观者细胞这是一种炎症炎症炎症炎症.

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