ISG20 inhibits bluetongue virus replication

文献类型： 外文期刊

第一作者： Kang, Di

作者： Kang, Di;Gao, Shandian;Tian, Zhancheng;Zhang, Guorui;Guan, Guiquan;Liu, Guangyuan;Luo, Jianxun;Du, Junzheng;Yin, Hong;Yin, Hong

作者机构：

关键词： Bluetongue virus (BTV); Interferon-stimulated genes (ISGs); Ovine ISG20; Virus replication; Antiviral immunity

期刊名称：VIROLOGICA SINICA （ 影响因子：6.947； 五年影响因子：5.997 ）

ISSN： 1674-0769

年卷期： 2022 年 37 卷 4 期

页码：

收录情况： SCI

摘要： ISG20 is an interferon-inducible exonuclease that inhibits virus replication. Although ISG20 is thought to degrade viral RNA, the antiviral mechanism and specificity of ISG20 remain unclear. In this study, the antiviral role of ovine ISG20 (oISG20) in bluetongue virus (BTV) infection was investigated. It was found that BTV infection up -regulated the transcription of ovine ISG20 (oISG20) in a time-and BTV multiplicity of infection (MOI)-dependent manner. Overexpression of oISG20 suppressed the production of BTV genome, proteins, and virus titer, whereas the knockdown of oISG20 increased viral replication. oISG20 was found to co-localize with BTV proteins VP4, VP5, VP6, and NS2, but only directly interacted with VP4. Exonuclease defective oISG20 significantly decreased the inhibitory effect on BTV replication. In addition, the interaction of mutant oISG20 and VP4 was weakened, suggesting that binding to VP4 was associated with the inhibition of BTV replication. The present data charac-terized the anti-BTV effect of oISG20, and provides a novel clue for further exploring the inhibition mechanism of double-stranded RNA virus by ISG20.

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