ArticleNature microbiology2025
Intragenic viral silencer element regulates HTLV-1 latency via RUNX complex recruitment.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed.
- Viral persistence and host-state remodeling in virus-associated cancers.Archives of microbiology · 2026Review
- Immunophenotype and proviral landscape of HTLV-1c infection and pulmonary disease.EBioMedicine · 2026Article
- Integrated TCRγ Clonality Workflow for Molecular Diagnosis in HTLV-1 Carriers and Adult T-Cell Leukemia/Lymphoma.Diagnostics (Basel, Switzerland) · 2026Article
- Virus infections and cancers: from mechanisms to therapeutics.Molecular biomedicine · 2026Review
- Immunological decoding of adult T cell leukemia - its cell of origin and oncogenesis.Biomarker research · 2026Review
- Review
- Viral-driven oncogenesis in T/NK-cell lymphomas: parallels and divergences between HTLV-1 and EBV.International journal of hematology · 2026Review
- Observational
- Review
- Intra-pol proviral open region of HTLV-1 controls the transcription from both long terminal repeats.Retrovirology · 2025Article
- Advances in clonality analysis of human T-cell leukemia virus type 1-infected cells: from Southern blotting to high-throughput sequencing.Journal of clinical and experimental hematopathology : JCEH · 2025Review
- The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex binding.Npj viruses · 2025Article
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.