TBK1 Mediates Innate Antiviral Immune Response against Duck Enteritis Virus

文献类型： 外文期刊

第一作者： Wang, Dongfang

作者： Wang, Dongfang;Huo, Hong;Werid, Gebremeskel Mamu;Ibrahim, Yassein M.;Wang, Yue;Chen, Hongyan;Wang, Dongfang;Tang, Lijie;Wang, Yue

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关键词： duck enteritis virus; antiviral immunity; TBK1; type I interferon

期刊名称：VIRUSES-BASEL （ 影响因子：5.818； 五年影响因子：5.811 ）

ISSN：

年卷期： 2022 年 14 卷 5 期

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收录情况： SCI

摘要： Duck enteritis virus (DEV) can infect several types of waterfowl can cause high mortality and huge economic losses to the global waterfowl industry. Type I interferons (IFN) are important for host defense against virus infection through induction of antiviral effector molecules. TANK-binding kinase 1 (TBK1) is a key kinase required for the induction of type I IFNs; however, the role of TBK1 on DEV infection remains unclear. Here, we observed that the expression levels of TBK1 and IFN-beta were upregulated during DEV infection in vivo and in vitro. Thus, the function of TBK1 on DEV infection was determined. The results showed that overexpression of TBK1 reduced DEV infection and knockdown of TBK1 resulted in the increased of DEV infection. Additionally, TBK1 overexpression upregulated the expression of IFN-beta and a few interferon-stimulated genes (ISGs), which thus inhibited the synthesis of DEV glycoprotein B. On the other hand, the TBK1 inhibitor Amlexanox down-regulated the expression levels of IFN-beta and IRF3. Interestingly, the expression levels of MAVS and GSK-3 beta were decreased in the cells treated with Amlexanox. Furthermore, overexpression of TBK1 activated the expression of upstream molecules MAVS and GSK-3 beta. Whereas, the expression of TBK1, IRF3 and IFN-beta was inhibited by the GSK-3 beta inhibitor SB216763. Our findings suggest that DEV-stimulated TBK1 may be involved in defense against DEV infection.

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