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IFI 16 regulates HTLV ‐1 replication through promoting HTLV ‐1 RTI ‐induced innate immune responses
Author(s) -
Yang Bo,
Song Di,
Liu Yue,
Cui Yuhan,
Lu Guangjian,
Di Wenyu,
Xing Hongxia,
Ma Lingling,
Guo Zhixiang,
Guan Yuhe,
Wang Hui,
Wang Jie
Publication year - 2018
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13077
Subject(s) - innate immune system , biology , gene knockdown , immune system , virology , retrovirus , viral replication , virus , immunology , microbiology and biotechnology , cell culture , genetics
Interferon ( IFN )‐inducible protein 16 ( IFI 16) 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 IFI 16 expression is induced by HTLV ‐1 infection or HTLV ‐1 reverse transcription intermediate ( RTI ) ss DNA 90 transfection. IFI 16 overexpression decreases HTLV ‐1 protein expression, whereas IFI 16 knockdown increases it. Furthermore, the knockdown of IFI 16 is followed by impaired innate immune responses upon HTLV ‐1 infection. In addition, IFI 16 forms a complex with ss DNA 90 and enhances ss DNA 90‐triggered innate immune responses. Collectively, our data suggest a critical role for IFI 16 during HTLV ‐1 infection by interacting with HTLV ‐1 RTI ss DNA 90 and restricting HTLV ‐1 replication.