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对排序的肺细胞的转录组分析揭示了NF-κB通路对SARS-CoV-2的前病毒活性

Anvita Bhargava¹, Ugo Szachnowski², Maxime Chazal¹

¹Institut Pasteur, Université de Paris, CNRS UMR 3569, Virus sensing and signaling Unit, 75015 Paris, France.

|January 12, 2024

概括

严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 感染大大减少细胞RNA,包括抗病毒因素. 然而,NF-κB途径促进病毒复制,而CYLD则抑制它.

科学领域:

* 分子生物学 * 分子生物学
* 病毒学病毒学
* 免疫学免疫学

背景情况:

*目前用于研究病毒感染的方法,如单细胞RNA测序,提供低分辨率的数据.
*在病毒感染期间精确解释基因表达,需要对受感染细胞进行高分辨率分析.

研究的目的:

* 进行SARS-CoV-2感染肺上皮细胞的深度转录组分析,按尖端 (S) 蛋白表达进行排序.
* 为了确定调节SARS-CoV-2复制在肺上皮细胞中的宿主因素.

主要方法:

*深度PolyA+转录组和SARS-CoV-2感染肺上皮细胞的新型RNA分析.
*基于病毒尖峰 (S) 蛋白表达的细胞分类.
*对已识别的途径和基因进行功能性研究.

主要成果:

*SARS-CoV-2感染导致信使RNAs (mRNAs) 和长非编码RNAs (lncRNAs) 的显著减少,包括干扰素 (IFN) 转录.
*尽管全球RNA减少,但S+细胞中NF-κB通路和炎症反应被上调.
*NF-κB途径显示出一种前病毒功能,而CYLD则表现出抗病毒活性.

结论:

*对被排序的感染细胞进行高分辨率的转录基因分析,揭示了关键的宿主-病原体相互作用.
*NF-κB通路和CYLD是肺上皮细胞中SARS-CoV-2复制的关键调节者.
* 准NF-κB通路或利用CYLD活动可能是针对SARS-CoV-2的潜在治疗策略.

关键词:

细胞细胞细胞文字转录学 (Transcriptomics) 是一个学科.病毒学病毒学

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