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-β 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-β 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-β and IRF3. Interestingly, the expression levels of MAVS and GSK-3β were decreased in the cells treated with
Amlexanox. Furthermore, overexpression of TBK1 activated the expression of upstream molecules MAVS and GSK-3β. Whereas, the expression of TBK1, IRF3 and IFN-β was inhibited by the GSK-3β inhibitor
SB216763. Our findings suggest that DEV-stimulated TBK1 may be involved in defense against DEV
infection.