IFI 16 regulates HTLV ‐1 replication through promoting HTLV ‐1 RTI ‐induced innate immune responses

作者：Bo Yang, Di Song, Yue Liu, Yuhan Cui, Guangjian Lu, Wenyu Di, Hongxia Xing, Lingling Ma, Zhixiang Guo, Yuhe Guan, Hui Wang, Jie Wang · 发表于：FEBS Letters · 年份：2018 · DOI：10.1002/1873-3468.13077 · 被引用次数：14 · 研究领域：T-cell and Retrovirus Studies、Viral Infections and Immunology Research、Animal Disease Management and Epidemiology

Interferon (IFN)-inducible protein 16 (IFI16) regulates human immunodeficiency virus replication by inducing innate immune responses as a DNA sensor. Human T-lymphotropic virus type 1 (HTLV-1), a delta retrovirus family member, has been linked to multiple diseases. Here, we report that IFI16 expression is induced by HTLV-1 infection or HTLV-1 reverse transcription intermediate (RTI) ssDNA90 transfection. IFI16 overexpression decreases HTLV-1 protein expression, whereas IFI16 knockdown increases it. Furthermore, the knockdown of IFI16 is followed by impaired innate immune responses upon HTLV-1 infection. In addition, IFI16 forms a complex with ssDNA90 and enhances ssDNA90-triggered innate immune responses. Collectively, our data suggest a critical role for IFI16 during HTLV-1 infection by interacting with HTLV-1 RTI ssDNA90 and restricting HTLV-1 replication.