AI Article Synopsis
- Duck hepatitis A virus genotype 3 (DHAV-3) significantly impacts the duck industry in China, leading to substantial economic losses.
- Research involved sequencing the whole transcriptome of susceptible and resistant Pekin ducklings at various time points post-infection, revealing thousands of differentially expressed genes, miRNAs, and lncRNAs.
- The study highlights the complex interactions of ncRNAs (non-coding RNAs) in regulating immune and metabolic responses during DHAV-3 infection, pointing to potential new treatment targets for infected ducks.
Article Abstract
As the most prevalent pathogen of duck viral hepatitis (DVH), duck hepatitis A virus genotype 3 (DHAV-3) has caused huge economic losses to the duck industry in China. Herein, we obtained whole-transcriptome sequencing data of susceptible (S) and resistant (R) Pekin duckling samples at 0 h, 12 h, and 24 h after DHAV-3 infection. We found that DHAV-3 infection induces 5,396 differentially expressed genes (DEGs), 85 differentially expressed miRNAs (DEMs), and 727 differentially expressed lncRNAs (DELs) at 24 hpi in S vs. R ducks, those upregulated genes were enriched in inflammation and cell communications pathways and downregulated genes were related to metabolic processes. Upregulated genes showed high connectivity with the miR-33, miR-193, and miR-11591, and downregulated genes were mainly regulated by miR-2954, miR-125, and miR-146b. With the construction of lncRNA-miRNA-mRNA axis, we further identified a few aberrantly expressed lncRNAs (e.g., MSTRG.36194.1, MSTRG.50601.1, MSTRG.34328.7, and MSTRG.29445.1) that regulate expression of hub genes (e.g., THBD, CLIC2, IL8, ACOX2, GPHN, SMLR1, and HAO1) by sponging those highly connected miRNAs. Altogether, our findings defined a dual role of ncRNAs in immune and metabolic regulation during DHAV-3 infection, suggesting potential new targets for treating DHAV-3 infected ducks.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10846394 | PMC |
| http://dx.doi.org/10.1016/j.psj.2023.103416 | DOI Listing |
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