Genome-wide identification of chicken bursae of Fabricius miRNAs in response to very virulent infectious bursal disease virus

被引:0
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作者
Xuewei Huang
Yue Li
Xiaona Wang
Junyan Zhang
Li Wang
Han Zhou
Yanping Jiang
Wen Cui
Xinyuan Qiao
Yijing Li
Lijie Tang
机构
[1] Northeast Agricultural University,College of Veterinary Medicine
[2] Qingdao Agricultural University,College of Veterinary Medicine
[3] Heilongjiang Key Laboratory for Animal Disease Control and Pharmaceutical Development,undefined
来源
Archives of Virology | 2022年 / 167卷
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摘要
Infectious bursal disease virus (IBDV) can cause a highly contagious immunosuppressive disease in young chickens. MicroRNAs (miRNAs) are crucial regulators of gene expression and are involved in the pathogenesis of IBDV infection. To investigate the roles of miRNA in chicken bursae of Fabricius in response to very virulent IBDV (vvIBDV) infection, RNA sequencing was performed to compare the small RNA libraries from uninfected and vvIBDV-infected group which was infected for 3 days. A total of 77 differentially expressed (DE) miRNAs were identified in BF, of which 42 DE miRNAs were upregulated and 35 DE miRNAs were downregulated. A gene ontology analysis showed that genes associated with cellular processes, cells, and binding were enriched. Moreover, pathway analyses suggested that apoptosis, T cell receptor signaling pathways, and chemokine signaling pathways may be activated following vvIBDV infection. In addition, we predicted the target genes of DE miRNAs and constructed an miRNA-mRNA regulatory network. In total, 189 pairs of miRNA-target genes were identified, comprising 67 DE miRNAs and 73 mRNAs. In this network, gga-miR-1684b-3p was identified with the highest fold change, as well as gga-miR-1788-3p and gga-miR-3530-5p showed a high degree of change. The above three miRNAs were considered to play vital roles in vvIBDV-host interactions. This study was the first to perform a comprehensive analysis of DE miRNAs in the bursa of Fabricius in response to vvIBDV infection, and it provided new insights into molecular mechanisms underlying vvIBDV infection and pathogenesis.
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页码:1855 / 1864
页数:9
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