ArticleProceedings of the National Academy of Sciences of the United States of America2015
TCF1 and LEF1 act as T-cell intrinsic HTLV-1 antagonists by targeting Tax.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Identification of AK4 and RHOC as potential oncogenes addicted by adult T cell leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A Review on Transcriptional Responses of Interactions between Insect Vectors and Plant Viruses.Cells · 2022Review
- Review
- TargetingFrontiers in immunology · 2021Article
- When Viruses Cross Developmental Pathways.Frontiers in cell and developmental biology · 2021Review
- Molecular biology of human T cell leukemia virus.Seminars in diagnostic pathology · 2020Review
- Immunopathogenesis and Cellular Interactions in Human T-Cell Leukemia Virus Type 1 Associated Myelopathy/Tropical Spastic Paraparesis.Frontiers in microbiology · 2020Review
- STLV-1 as a model for studying HTLV-1 infection.Retrovirology · 2019Review
- Pentosan Polysulfate Demonstrates Anti-human T-Cell Leukemia Virus Type 1 ActivitiesJournal of virology · 2019Article
- Histone H2A monoubiquitylation and p38-MAPKs regulate immediate-early gene-like reactivation of latent retrovirus HTLV-1.JCI insight · 2018Article
- HTLV-1 Alters T Cells for Viral Persistence and Transmission.Frontiers in microbiology · 2018Review
- HTLV-1: Regulating the Balance Between Proviral Latency and Reactivation.Frontiers in microbiology · 2018Review
- Human T-cell leukaemia virus type 1: parasitism and pathogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Article
- The sense behind retroviral anti-sense transcription.Virology journal · 2017Article
- Gene expression profiling of hematologic malignant cell lines resistant to oncolytic virus treatment.Oncotarget · 2017Article
- HTLV-1 bZIP Factor Enhances T-Cell Proliferation by Impeding the Suppressive Signaling of Co-inhibitory Receptors.PLoS pathogens · 2017Article
- Multifaceted functions and roles of HBZ in HTLV-1 pathogenesis.Retrovirology · 2016Review
- Molecular Studies of HTLV-1 Replication: An Update.Viruses · 2016Review
- How does HTLV-1 cause adult T-cell leukaemia/lymphoma (ATL)?Current opinion in virology · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) is a delta-type retrovirus that induces malignant and inflammatory diseases during its long persistence in vivo. HTLV-1 can infect various kinds of cells; however, HTLV-1 provirus is predominantly found in peripheral CD4 T cells in vivo. Here we find that TCF1 and LEF1, two Wnt transcription factors that are specifically expressed in T cells, inhibit viral replication through antagonizing Tax functions. TCF1 and LEF1 can each interact with Tax and inhibit Tax-dependent viral expression and activation of NF-κB and AP-1. As a result, HTLV-1 replication is suppressed in the presence of either TCF1 or LEF1. On the other hand, T-cell activation suppresses the expression of both TCF1 and LEF1, and this suppression enables Tax to function as an activator. We analyzed the thymus of a simian T-cell leukemia virus type 1 (STLV-1) infected Japanese macaque, and found a negative correlation between proviral load and TCF1/LEF1 expression in various T-cell subsets, supporting the idea that TCF1 and LEF1 negatively regulate HTLV-1 replication and the proliferation of infected cells. Thus, this study identified TCF1 and LEF1 as Tax antagonistic factors in vivo, a fact which may critically influence the peripheral T-cell tropism of this virus.
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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 OpenQuestion graph.