MicroRNA gga-miR-130b Suppresses Infectious Bursal Disease Virus Replication via Targeting of the Viral Genome and Cellular Suppressors of Cytokine Signaling 5

被引:52
作者
Fu, Mengjiao [1 ,2 ,3 ]
Wang, Bin [1 ,2 ,3 ]
Chen, Xiang [1 ,2 ,3 ]
He, Zhiyuan [1 ,2 ,3 ]
Wang, Yongqiang [1 ,2 ,3 ]
Li, Xiaoqi [3 ]
Cao, Hong [1 ,2 ,3 ]
Zheng, Shijun J. [1 ,2 ,3 ]
机构
[1] State Key Lab Agrobiotechnol, Beijing, Peoples R China
[2] Minist Agr, Key Lab Anim Epidemiol & Zoonosis, Beijing, Peoples R China
[3] China Agr Univ, Coll Vet Med, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
microRNA; type I IFN; IBDV; SOCS; LARGE RNA SEGMENT; NF-KAPPA-B; EXPRESSION; PROTEINS; CELLS; PROLIFERATION; ACTIVATION; INHIBITION; FAMILY; VP1;
D O I
10.1128/JVI.01646-17
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression posttranscriptionally through silencing or degrading their targets, thus playing important roles in the immune response. However, the role of miRNAs in the host response against infectious bursal disease virus (IBDV) infection is not clear. In this study, we show that the expression of a series of miRNAs was significantly altered in DF-1 cells after IBDV infection. We found that the miRNA gga-miR-130b in-hibited IBDV replication via targeting the specific sequence of IBDV segment A and enhanced the expression of beta interferon (IFN-beta) by targeting suppressors of cytokine signaling 5 (SOCS5) in host cells. These findings indicate that gga-miR130b-3p plays a crucial role in host defense against IBDV infection. IMPORTANCE This work shows that gga-miR-130b suppresses IBDV replication via directly targeting the viral genome and cellular SOCS5, the negative regulator for type I interferon expression, revealing the mechanism underlying gga-miR-130-induced inhibition of IBDV replication. This information will be helpful for the understanding of how host cells combat pathogenic infection by self-encoded small RNA and furthers our knowledge of the role of microRNAs in the cell response to viral infection.
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页数:15
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