ArticleRetrovirology2015
HTLV-1 drives vigorous clonal expansion of infected CD8(+) T cells in natural infection.
Article in Retrovirology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed.
- ERVK activity in CD8Journal of neuroinflammation · 2026Article
- Virus-host immune interaction in asymptomatic HTLV-1 carriers.Microbiology spectrum · 2025Article
- The Assembly of HTLV-1-How Does It Differ from HIV-1?Viruses · 2024Review
- IncreasedInternational journal of molecular sciences · 2024Article
- HTLV-1 induces an inflammatory CD4+CD8+ T cell population in HTLV-1-associated myelopathy.JCI insight · 2024Article
- Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets.International journal of molecular sciences · 2023Review
- Article
- Article
- Review
- Selective clonal persistence of human retroviruses in vivo: Radial chromatin organization, integration site, and host transcription.Science advances · 2022Article
- Regulation of HTLV-1 transformation.Bioscience reports · 2022Review
- Latency Reversing Agents: Kick and Kill of HTLV-1?International journal of molecular sciences · 2021Review
- A novel positive feedback-loop between the HTLV-1 oncoprotein Tax and NF-κB activity in T-cells.Retrovirology · 2020Article
- Transfer of HTLV-1 p8 and Gag to target T-cells depends on VASP, a novel interaction partner of p8.PLoS pathogens · 2020Article
- Human T leukaemia Type 1 and COVID-19.Pathogens (Basel, Switzerland) · 2020Article
- Inhibition of IκBα phosphorylation potentiates regulated cell death induced by azidothymidine in HTLV-1 infected cells.Cell death discovery · 2020Article
- Immunopathogenesis and Cellular Interactions in Human T-Cell Leukemia Virus Type 1 Associated Myelopathy/Tropical Spastic Paraparesis.Frontiers in microbiology · 2020Review
- Collagen IV (COL4A1, COL4A2), a Component of the Viral Biofilm, Is Induced by the HTLV-1 Oncoprotein Tax and Impacts Virus Transmission.Frontiers in microbiology · 2019Article
- Post-transcriptional Regulation of HTLV Gene Expression: Rex to the Rescue.Frontiers in microbiology · 2019Review
- Switching and loss of cellular cytokine producing capacity characterize in vivo viral infection and malignant transformation in human T- lymphotropic virus type 1 infection.PLoS pathogens · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundHuman T-lymphotropic Virus Type I (HTLV-1) is a retrovirus that persistently infects 5-10 million individuals worldwide and causes disabling or fatal inflammatory and malignant diseases. The majority of the HTLV-1 proviral load is found in CD4(+) T cells, and the phenotype of adult T cell leukemia (ATL) is typically CD4(+). HTLV-1 also infects CD8(+) cells in vivo, but the relative abundance and clonal composition of the two infected subpopulations have not been studied. We used a high-throughput DNA sequencing protocol to map and quantify HTLV-1 proviral integration sites in separated populations of CD4(+) cells, CD8(+) cells and unsorted peripheral blood mononuclear cells from 12 HTLV-1-infected individuals.
resultsWe show that the infected CD8(+) cells constitute a median of 5% of the HTLV-1 proviral load. However, HTLV-1-infected CD8(+) clones undergo much greater oligoclonal proliferation than the infected CD4(+) clones in infected individuals, regardless of disease manifestation. The CD8(+) clones are over-represented among the most abundant clones in the blood and are redetected even after several years.
conclusionsWe conclude that although they make up only 5% of the proviral load, the HTLV-1-infected CD8(+) T-cells make a major impact on the clonal composition of HTLV-1-infected cells in the blood. The greater degree of oligoclonal expansion observed in the infected CD8(+) T cells, contrasts with the CD4(+) phenotype of ATL; cases of CD8(+) adult T-cell leukaemia/lymphoma are rare. This work is consistent with growing evidence that oligoclonal expansion of HTLV-1-infected cells is not sufficient for malignant transformation.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.