The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex binding

A defining feature of Human T-cell leukaemia virus type 1 (HTLV-1) infection is the establishment of reversible latency that can persist for many years. This latency enables the expansion of infected CD4+ T cells, ultimately contributing to adult T-cell leukaemia (ATL) and inflammatory disease. Suga...

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Main Authors: Natasha Jansz, Damian F. J. Purcell
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:npj Viruses
Online Access:https://doi.org/10.1038/s44298-025-00136-7
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author Natasha Jansz
Damian F. J. Purcell
author_facet Natasha Jansz
Damian F. J. Purcell
author_sort Natasha Jansz
collection DOAJ
description A defining feature of Human T-cell leukaemia virus type 1 (HTLV-1) infection is the establishment of reversible latency that can persist for many years. This latency enables the expansion of infected CD4+ T cells, ultimately contributing to adult T-cell leukaemia (ATL) and inflammatory disease. Sugata et al. identify a viral negative regulatory element within the HTLV-1 proviral genome that governs transcriptional latency. This intragenic silencing element contains binding sites for the master haematopoietic transcription factor, RUNX1. RUNX1 complex binding represses viral expression, thereby reducing viral production, antigen presentation, and susceptibility to cytotoxic T lymphocyte responses. The intragenic silencing element described in their study is unique to HTLV-1 and represents a novel strategy by which the virus achieves lifelong persistence in the host.
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spelling doaj-art-594ebd94ab5940bf884e2aecabbf40522025-08-20T03:42:40ZengNature Portfolionpj Viruses2948-17672025-07-01311310.1038/s44298-025-00136-7The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex bindingNatasha Jansz0Damian F. J. Purcell1Department of Microbiology and Immunology, The University of Melbourne at the Peter Doherty Institute for Infection and ImmunityDepartment of Microbiology and Immunology, The University of Melbourne at the Peter Doherty Institute for Infection and ImmunityA defining feature of Human T-cell leukaemia virus type 1 (HTLV-1) infection is the establishment of reversible latency that can persist for many years. This latency enables the expansion of infected CD4+ T cells, ultimately contributing to adult T-cell leukaemia (ATL) and inflammatory disease. Sugata et al. identify a viral negative regulatory element within the HTLV-1 proviral genome that governs transcriptional latency. This intragenic silencing element contains binding sites for the master haematopoietic transcription factor, RUNX1. RUNX1 complex binding represses viral expression, thereby reducing viral production, antigen presentation, and susceptibility to cytotoxic T lymphocyte responses. The intragenic silencing element described in their study is unique to HTLV-1 and represents a novel strategy by which the virus achieves lifelong persistence in the host.https://doi.org/10.1038/s44298-025-00136-7
spellingShingle Natasha Jansz
Damian F. J. Purcell
The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex binding
npj Viruses
title The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex binding
title_full The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex binding
title_fullStr The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex binding
title_full_unstemmed The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex binding
title_short The silence within: a conserved intragenic silencing element governs HTLV-1 expression via host RUNX1 complex binding
title_sort silence within a conserved intragenic silencing element governs htlv 1 expression via host runx1 complex binding
url https://doi.org/10.1038/s44298-025-00136-7
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