AI Article Synopsis
- The study focused on how epigenetic mechanisms influence the expression of HTLV-1 Tax.
- The use of trichostatin A (TSA) to inhibit histone deacetylation led to increased Tax expression and histone hyperacetylation at the virus's LTR.
- HDACs, particularly HDAC1 and HDAC3, were shown to play a role in repressing Tax transcription, although the presence of HDAC activity was not strictly necessary for this repression.
Article Abstract
We examined the epigenetic mechanisms involved in human T-cell lymphotropic virus type 1 (HTLV-1) Tax expression. Blockade of histone deacetylation with trichostatin A (TSA) resulted in Tax upregulation. Using a chromatin immunoprecipitation (ChIP) assay, we verified local histone hyperacetylation at the HTLV-1 LTR in response to TSA. In agreement, HDAC3 transfection led to reductions in both Tax expression and histone acetylation. HDAC3 mutations and deletions spanning the catalytic site had variable ability to repress Tax, but HDAC activity was not essential for repression. Immunoprecipitation studies revealed that Tax co-exists in a complex containing both histone deacetylase 1 (HDAC1) and 3 (HDAC3). Our results suggest that HDACs may actively participate in the repression of HTLV-1 Tax transcription.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Recent progress in pathological understanding of adult T-cell leukemia/lymphoma in the new classification era.
Leuk Res
December 2024
Laboratory of Hemato-Immunology, Graduate School of Health Sciences, University of the Ryukyus, Nishihara, Japan.
Article Synopsis
- Adult T-cell leukemia/lymphoma (ATLL) is a type of cancer linked to HTLV-1 virus infection, with the WHO's new 5th Edition classification outlining essential and desirable diagnostic criteria for its identification.
- A new diagnostic method combining HBZ-ISH and tax-PCR enhances detection of HTLV-1 in cases where only preserved tissue samples are available, alongside traditional Southern blot techniques.
- The review addresses the morphological and phenotypic characteristics of ATLL, noting the prevalence of certain phenotypes, genetic abnormalities, and emphasizing the need for further research and classification in understanding the disease's complex nature.
Immunological aspects of HTLV-1 persistence; for the prevention and treatment of Adult T-cell leukaemia-lymphoma (ATL).
Leuk Res
December 2024
National Centre for Human Retrovirology and Department of Haematology, Imperial College Healthcare NHS Trust, UK; Department of Immunology & Inflammation, Imperial College London, UK. Electronic address:
Human T-cell leukaemia virus type-1 (HTLV-1) causes the highly aggressive malignancy adult T-cell leukaemia-lymphoma (ATL) in approximately 5 % of chronically infected carriers. HTLV-1 persists in the host by enhancing survival of infected-T-cells despite the presence of a strong immune response. Therefore, asymptomatic HTLV-1 carriers have a lifelong balance between infected cell proliferation and the host antiviral immune response.
View Article and Find Full Text PDFCharacterization of HTLV-1 Infectious Molecular Clone Isolated from Patient with HAM/TSP and Immortalization of Human Primary T-Cell Lines.
Viruses
November 2024
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160, USA.
Article Synopsis
- HTLV-1 is linked to diseases like adult T-cell leukemia and HTLV-1-associated myelopathy, prompting researchers to isolate a molecular clone from a patient with HAM/TSP.
- This clone exhibits unique genetic features and viral mRNA patterns, indicating a potential connection to the development of HAM/TSP.
- The study finds that while direct infection of primary T cells with HTLV-1 clones leads to limited cell growth, transmission from dendritic cells enhances long-term proliferation and supports latent infections.
A Novel Tax-Responsive Reporter T-Cell Line to Analyze Infection of HTLV-1.
Pathogens
November 2024
Institute of Clinical and Molecular Virology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91054 Erlangen, Germany.
Human T-cell leukemia virus type 1 (HTLV-1) infects CD4 T-cells through close cell-cell contacts. The viral Tax-1 (Tax) protein regulates transcription by transactivating the HTLV-1 promoter in the 5' long terminal repeat of the integrated provirus. Here, we generated a clonal Tax-responsive T-cell line to track HTLV-1 infection at the single-cell level using flow cytometry, bypassing intracellular viral protein staining.
View Article and Find Full Text PDFRewired chromatin structure and epigenetic gene dysregulation during HTLV-1 infection to leukemogenesis.
Cancer Sci
November 2024
Laboratory of Viral Oncology and Genomics, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan.
Human T-cell leukemia virus type 1 (HTLV-1) broadly impacts host genes, affecting the infected cell population and inducing the development of a disease with a poor prognosis, adult T-cell leukemia-lymphoma (ATL). This study aimed to provide a comprehensive epigenomic characterization of the infected cell population and evaluated the transcriptome and chromatin structures of peripheral blood cells in HTLV-1-infected individuals using RNA sequencing (RNA-seq) and assay for transposase-accessible chromatin sequencing (ATAC-seq). The infected cells showed significant changes in gene expression patterns from the polyclonal stage and before ATL onset while demonstrating similarities to tumor-forming ATL cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!