对感染PDCoV的HIEC-6细胞和丰富途径PI3K-Akt和P38 MAPK的转录组分析

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Updated: Jun 27, 2025

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Yuhang Jiang^1,2, Guoqing Zhang², Letian Li²

¹College of Veterinary Medicine, Northwest A&F University, Xianyang 712100, China.

|April 27, 2024

概括

猪甲型冠状病毒 (PDCoV) 感染人类肠道细胞,改变基因表达. 针对PI3K-Akt和P38 MAPK通路显示了预防PDCoV感染的潜力.

科学领域:

病毒学病毒学
分子生物学分子生物学
基因组学就是基因组学.

背景情况:

猪三角型冠状病毒 (PDCoV) 在小猪中引起肠道疾病.
关于PDCoV与人类细胞相互作用的知识有限.

研究的目的:

研究PDCoV与人类肠道细胞 (HIEC-6) 的相互作用.
在感染后12,24和48小时分析转录组变化.
确定PDCoV感染的潜在治疗点.

主要方法:

对感染PDCoV. 6的HIEC-6细胞的转录组分析.
在多个时间点进行差异基因表达分析.
进行KEGG通路分析并识别关键基因 (例如BUB1,DDIT4,ATF3,GBP2,IRF1).

主要成果:

在所有时间点中都发现了大量的差异表达基因 (DEGs).
常见的DEG在细胞因子生产和信号通路 (p53,PI3K-Akt,TNF) 中得到了丰富.
24小时后,PI3K-Akt和P38 MAPK通路显著丰富,EFNA1和KITLG被确定为关键基因. 这些途径的抑制增强了PDCoV感染.

结论:

感染PDCoV会导致人类肠道细胞的显著转录变化.
PI3K-Akt和P38 MAPK信号通路对于PDCoV感染至关重要.
EFNA1和KITLG可以作为PDCoV感染的治疗点.

关键词:

P38 MAPK 路径中的一个.通过PI3K-Akt路径.冠状病毒冠状病毒病毒猪三角洲冠状病毒病毒转录组 (transcriptome) 是一个转录组.

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