論文種別	原著(症例報告除く)
言語種別	英語
査読の有無	査読あり
表題	Intragenic viral silencer element regulates HTLV-1 latency via RUNX complex recruitment
掲載誌名	正式名：Nature microbiology 略　 称：Nat Microbiol ISSNコード：20585276/20585276
掲載区分	国外
巻・号・頁	10(6),pp.1447-1462
著者・共著者	Kenji Sugata, Akhinur Rahman, Koki Niimura, Kazuaki Monde, Takaharu Ueno, Samiul Alam Rajib, Mitsuyoshi Takatori, Wajihah Sakhor, Md Belal Hossain, Sharmin Nahar Sithi, M Ishrat Jahan, Kouki Matsuda, Mitsuharu Ueda, Yoshihisa Yamano, Terumasa Ikeda, Takamasa Ueno, Kiyoto Tsuchiya, Yuetsu Tanaka, Masahito Tokunaga, Kenji Maeda, Atae Utsunomiya, Kazu Okuma, Masahiro Ono, Yorifumi Satou
発行年月	2025/06
概要	Retroviruses integrate their genetic material into the host genome, enabling persistent infection. Human T cell leukaemia virus type 1 (HTLV-1) and human immunodeficiency virus type 1 (HIV-1) share similarities in genome structure and target cells, yet their infection dynamics differ drastically. While HIV-1 leads to high viral replication and immune system collapse, HTLV-1 establishes latency, promoting the survival of infected cells and, in some cases, leading to leukaemia. The mechanisms underlying this latency preference remain unclear. Here we analyse blood samples from people with HTLV-1 and identify an open chromatin region within the HTLV-1 provirus that functions as a transcriptional silencer and regulates transcriptional burst. The host transcription factor RUNX1 binds to this open chromatin region, repressing viral expression. Mutation of this silencer enhances HTLV-1 replication and immunogenicity, while its insertion into HIV-1 suppresses viral production. These findings reveal a strategy by which HTLV-1 ensures long-term persistence, offering potential insights into retroviral evolution and therapeutic targets.
DOI	10.1038/s41564-025-02006-7
PMID	40360701