MicroRNA-23b Promotes Avian Leukosis Virus Subgroup J (ALV-J) Replication by Targeting IRF1

文献类型： 外文期刊

第一作者： Li, Zhenhui

作者： Li, Zhenhui;Chen, Biao;Feng, Min;Ouyang, Hongjia;Zheng, Ming;Ye, Qiao;Nie, Qinghua;Zhang, Xiquan;Li, Zhenhui;Chen, Biao;Feng, Min;Ouyang, Hongjia;Zheng, Ming;Ye, Qiao;Nie, Qinghua;Zhang, Xiquan;Li, Zhenhui;Chen, Biao;Feng, Min;Ouyang, Hongjia;Zheng, Ming;Ye, Qiao;Nie, Qinghua;Zhang, Xiquan

作者机构：

期刊名称：SCIENTIFIC REPORTS （ 影响因子：4.379； 五年影响因子：5.133 ）

ISSN： 2045-2322

年卷期： 2015 年 5 卷

页码：

收录情况： SCI

摘要： Avian leukosis virus subgroup J (ALV-J) can cause several different leukemia-like proliferative diseases in the hemopoietic system of chickens. Here, we investigated the transcriptome profiles and miRNA expression profiles of ALV-J-infected and uninfected chicken spleens to identify the genes and miRNAs related to ALV-J invasion. In total, 252 genes and 167 miRNAs were differentially expressed in ALV-J-infected spleens compared to control uninfected spleens. miR-23b expression was up-regulated in ALV-J-infected spleens compared with the control spleens, and transcriptome analysis revealed that the expression of interferon regulatory factor 1 (IRF1) was down-regulated in ALV-J-infected spleens compared to uninfected spleens. A dual-luciferase reporter assay showed that IRF1 was a direct target of miR-23b. miR-23b overexpression significantly (P = 0.0022) decreased IRF1 mRNA levels and repressed IRF1-3'-UTR reporter activity. In vitro experiments revealed that miR-23b overexpression strengthened ALV-J replication, whereas miR-23b loss of function inhibited ALV-J replication. IRF1 overexpression inhibited ALV-J replication, and IRF1 knockdown enhanced ALV-J replication. Moreover, IRF1 overexpression significantly (P = 0.0014) increased IFN-beta expression. In conclusion, these results suggested that miR-23b may play an important role in ALV-J replication by targeting IRF1.

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