Li Guanghao, Feng Tingting, Pan Wen, Shi Xiaohong, Dai Jianfeng
Institute of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou City, Jiangsu Province, People's Republic of China.
Institute of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou City, Jiangsu Province, People's Republic of China.
Biochem Biophys Res Commun. 2015 Jan 2;456(1):327-32. doi: 10.1016/j.bbrc.2014.11.080. Epub 2014 Nov 28.
Dengue virus (DENV) is a mosquito-borne virus that threatens approximately 2.5 billion people worldwide. Vaccines against DENV are currently unavailable. DEAD-box RNA helicases (DDXs) have been reported to participate in viral replication and host innate immune response. In the present study, we analyzed the role of 40 DDX proteins during DENV replication. Among these proteins, DDX3X showed antiviral effect against DENV infection. Viral replication significantly increased in DDX3X-silenced cells compared with the controls. The interferon (IFN)-β transcription level decreased during the early stage of DENV infection in DDX3X-silenced cells compared with that in the controls. DDX3X could stimulate IFN-β transcription through the IRF3 and the NFκB branches in DENV-infected cells. Our data imply that DDX3X, a member of DEAD-box RNA helicase, is necessary for IFN production and could inhibit DENV replication.
登革病毒（DENV）是一种通过蚊子传播的病毒，全球约有25亿人受到其威胁。目前尚无针对登革病毒的疫苗。据报道，DEAD盒RNA解旋酶（DDXs）参与病毒复制和宿主固有免疫反应。在本研究中，我们分析了40种DDX蛋白在登革病毒复制过程中的作用。在这些蛋白中，DDX3X对登革病毒感染显示出抗病毒作用。与对照组相比，DDX3X沉默细胞中的病毒复制显著增加。与对照组相比，在DDX3X沉默细胞中登革病毒感染早期干扰素（IFN）-β转录水平下降。DDX3X可通过IRF3和NFκB分支刺激登革病毒感染细胞中的IFN-β转录。我们的数据表明，DEAD盒RNA解旋酶成员DDX3X是产生IFN所必需的，并且可以抑制登革病毒复制。
