IFI16 regulates HTLV-1 replication through promoting HTLV-1 RTI-induced innate immune responses

IFI16 通过促进 HTLV-1 RTI 诱导的先天免疫反应来调节 HTLV-1 复制

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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

Abstract

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.

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