ATG7/GAPLINC/IRF3轴在调节甲型流感病毒的病变发生方面发挥着至关重要的作用
Biao Chen1,2, Guijie Guo1,3, Guoqing Wang1,3
1Key Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, People's Republic of China.
PLoS pathogens
|January 16, 2024
概括
自相关蛋白7 (ATG7) 通过自依赖和独立的途径促进流感A病毒 (IAV) 复制. ATG7通过通过长非编码RNA GAPLINC和IRF3激活来抑制干扰素的产生来抑制天生的免疫力.
科学领域:
- 病毒学和免疫学 病毒学和免疫学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 自相关蛋白7 (ATG7) 对于自至关重要,自是一种涉及病毒感染的过程.
- 在A型流感病毒 (IAV) 感染和发病过程中,ATG7的特定作用和机制尚不清楚.
研究的目的:
- 阐明ATG7在IAV复制和发病过程中的功能和潜在机制.
- 研究ATG7在病毒感染中的自依赖性和独立性作用.
主要方法:
- 在体外研究涉及ATG7耗尽和过度表达.
- 使用了ATG7条件淘汰赛小鼠,这些小鼠受到IAV和伪狂犬病病毒的挑战.
- 转录组分析,干扰素测定,IRF3激活研究和lncRNAGAPLINC识别.
主要成果:
- ATG7 枯竭减弱了 IAV 复制,而过度表达增强了它.
- ATG7通过自依赖和独立的途径促进IAV复制.
- ATG7抑制了I型和III型干扰素的产生和IRF3的激活,由lncRNA GAPLINC.中介.
结论:
- ATG7在促进IAV复制和病原发生方面发挥着重要作用.
- 一个自独立的机制涉及ATG7通过ATG7/GAPLINC/IRF3轴抑制宿主天生的免疫力.
- 这项研究揭示了一种新的途径,在IAV感染期间调节抗病毒免疫力.
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