IFI16 regulates HTLV‐1 replication through promoting HTLV‐1 RTI‐induced innate immune responses. Issue 10 (14th May 2018)

• Record Type: Journal Article
• Authors: Yang, Bo; Song, Di; Liu, Yue; Cui, Yuhan; Lu, Guangjian; Di, Wenyu; Xing, Hongxia; Ma, Lingling; Guo, Zhixiang; Guan, Yuhe; Wang, Hui; Wang, Jie
• Is Part Of: FEBS letters. Volume 592:Issue 10(2018)
• Page Start: 1693
• Page End: 1704
• Publication Date: 2018-05-14
• Subjects: DNA sensor -- HTLV‐1 -- IFI16 -- innate immune responses -- reverse transcription intermediate; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1002/1873-3468.13077
• Languages: English
• ISSNs: 0014-5793

Abstract

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. Abstract :