DDX56 cooperates with FMDV 3A to enhance FMDV replication by inhibiting the phosphorylation of IRF3
文献类型： 外文期刊
第一作者： Fu, Shao-zu
作者： Fu, Shao-zu;Yang, Wen-ping;Ru, Yi;Zhang, Ke-shan;Wang, Yong;Liu, Xiang-tao;Li, Dan;Zheng, Hai-xue
作者机构：
关键词： DDX56; FMDV 3A; IRF3; Phosphorylation; Replication
期刊名称：CELLULAR SIGNALLING （ 影响因子：4.315； 五年影响因子：4.206 ）
ISSN： 0898-6568
年卷期： 2019 年 64 卷
页码：
收录情况： SCI
摘要： The components of foot-and-mouth disease virus (FMDV) interact with host cellular proteins to promote self-replication and evade the host immune response. Previous studies have shown that FMDV 3A, 2C and 2B proteins interact with host cellular proteins involved in FMDV replication. However, whether the other host proteins have an impact on FMDV replication is less understood. In this study, we identified DDX56 as a positive regulator of FMDV replication. DDX56 overexpression increased FMDV replication, whereas DDX56 knockdown had the opposite effect. DDX56 interacted and cooperated with FMDV 3A to inhibit the type I interferon by reducing the phosphorylation of IRF3. Moreover, the D166 site of DDX56 played a role in increasing FMDV replication and cooperating with FMDV 3A to inhibit the phosphorylation of IRF3. Additionally, knockdown of DDX56 or FMDV 3A results also showed that DDX56 cooperated with FMDV 3A to inhibit the phosphorylation of IRF3. These results suggest that the interaction between FMDV 3A protein and the host protein DDX56 is critical for FMDV replication.
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