Host factor DUSP5 potently inhibits dengue virus infection by modulating cytoskeleton rearrangement.
Host factor DUSP5 potently inhibits dengue virus infection by modulating cytoskeleton rearrangement.
复制标题
宿主因子DUSP5通过调节细胞骨架重排有效抑制登革病毒感染。
DOI：
10.1016/j.antiviral.2023.105622
复制
发表时间：
2023-05
影响因子：
7.6
通讯作者：
Minqi Liang;Yizhe Li;Kexin Zhang;Yujia Zhu;Jingyao Liang;Minjie Liu;Shuqing Zhang;Delin Chen-Del
中科院分区：
文献类型：
--
作者：
Minqi Liang;Yizhe Li;Kexin Zhang;Yujia Zhu;Jingyao Liang;Minjie Liu;Shuqing Zhang;Delin Chen-Del
Cytoskeleton has been reported to play an essential role in facilitating the viral life cycle. However, whether the host can exert its antiviral effects by modulating the cytoskeleton is not fully understood. In this study, we identified that host factor DUSP5 was upregulated after dengue virus (DENV) infection. In addition, we demonstrated that overexpression of DUSP5 remarkably inhibited DENV replication. Conversely, the depletion of DUSP5 led to an increase in viral replication. Moreover, DUSP5 was found to restrain viral entry into host cells by suppressing F-actin rearrangement via negatively regulating the ERK-MLCK-Myosin IIB signaling axis. Depletion of dephosphorylase activity of DUSP5 abolished its above inhibitory effects. Furthermore, we also revealed that DUSP5 exhibited broad-spectrum antiviral effects against DENV and Zika virus. Taken together, our studies identified DUSP5 as a key host defense factor against viral infection and uncovered an intriguing mechanism by which the host exerts its antiviral effects through targeting cytoskeleton rearrangement.
