DDX50 inhibits the replication of dengue virus 2 by upregulating IFN-β production

DDX50 通过上调 IFN-β 的产生来抑制登革热病毒 2 的复制

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作者:Peijun Han, Wei Ye, Xin Lv, Hongwei Ma, Daihui Weng, Yangchao Dong, Linfeng Cheng, Hesong Chen, Liang Zhang, Zhikai Xu, Yingfeng Lei, Fanglin Zhang

Abstract

Dengue virus (DENV) infects approximately 390 million people per year, and each of the four DENV serotypes (DENV-1, DENV-2, DENV-3, and DENV-4) is capable of causing infection. At present, there is no antiviral drug available for the treatment of DENV. Several DExD/H-box helicases have been shown to be involved in the antiviral immune response or viral replication. In the present study, we investigated the role of DDX50 in DENV-2 RNA replication. Our data showed that the level of DENV-2 RNA increased in DDX50 knockdown cells during an early stage of viral infection and decreased in DDX50-overexpressing cells. DDX50, in conjunction with RIG-I and MDA5, upregulated the production of IFN-β in infected cells through an additive effect on the IFN-β promoter. Furthermore, transcription of several IFN-stimulated genes was increased in DDX50-overexpressing cells infected with DENV-2. These results provide evidence that DDX50 negatively regulates DENV-2 replication during the early stages of infection by inducing IFN-β production.

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