International journal of medical microbiology : IJMM · 2025
DDX17 promotes DENV-2 replication via interaction with viral dsRNA and G3BP1.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Han Peijun, Ye Wei, Ma Hongwei, Dong Yangchao, Lv Xin, Liu He, Cheng Linfeng, Zhang Liang, Li Sumin, Lei Yingfeng, Zhang Fanglin
Аннотация
Dengue virus (DENV) is one of the major arboviruses that pose a serious threat to global human health. However, there is currently no specific antiviral drug available for the treatment of DENV infection. DDX17, a member of the DExD/H-box helicase family, has been implicated in the replication processes of various viruses. Our research group discovered that during the early stages of dengue virus replication, DDX17 promotes viral replication and suppresses the activity of the IFN promoter. Furthermore, DDX17 binds to viral dsRNA and interacts with G3BP1, a component of stress granules (SGs), to inhibit SG formation, thereby enhancing viral replication. By elucidating the role of DDX17 in the early stages of dengue virus replication, our findings provide valuable insights into host-pathogen interactions during DENV infection, offering potential therapeutic perspectives.