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High-Throughput Transcriptome Analysis for Investigating Host-Pathogen Interactions
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Transcriptomic Analysis of PDCoV-Infected HIEC-6 Cells and Enrichment Pathways PI3K-Akt and P38 MAPK
Yuhang Jiang1,2, Guoqing Zhang2, Letian Li2
1College of Veterinary Medicine, Northwest A&F University, Xianyang 712100, China.
Viruses
|April 27, 2024
Summary
Porcine Deltacoronavirus (PDCoV) infects human intestinal cells, altering gene expression. Targeting PI3K-Akt and P38 MAPK pathways shows potential for preventing PDCoV infection.
Area of Science:
- Virology
- Molecular Biology
- Genomics
Background:
- Porcine Deltacoronavirus (PDCoV) causes intestinal disease in piglets.
- Limited knowledge exists on PDCoV interactions with human cells.
Purpose of the Study:
- Investigate PDCoV interactions with human intestinal cells (HIEC-6).
- Analyze transcriptome changes at 12, 24, and 48 hours post-infection.
- Identify potential therapeutic targets for PDCoV infection.
Main Methods:
- Transcriptome analysis of HIEC-6 cells infected with PDCoV.
- Differential gene expression analysis at multiple time points.
- KEGG pathway analysis and identification of key genes (e.g., BUB1, DDIT4, ATF3, GBP2, IRF1).
Main Results:
- Significant numbers of differentially expressed genes (DEGs) were identified at all time points.
- Common DEGs were enriched in cytokine production and signaling pathways (p53, PI3K-Akt, TNF).
- PI3K-Akt and P38 MAPK pathways were significantly enriched at 24 hours, with EFNA1 and KITLG identified as key genes. Inhibition of these pathways enhanced PDCoV infection.
Conclusions:
- PDCoV infection induces significant transcriptional changes in human intestinal cells.
- The PI3K-Akt and P38 MAPK signaling pathways are crucial for PDCoV infection.
- EFNA1 and KITLG may serve as therapeutic targets for PDCoV infection.
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