Evidence map›Paper›PMID 26929370›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

The retrovirus HTLV-1 inserts an ectopic CTCF-binding site into the human genome.

Yorifumi Satou, Paola Miyazato, Ko Ishihara, Hiroko Yaguchi, Anat Melamed, Michi Miura, Asami Fukuda, Kisato Nosaka, Takehisa Watanabe, Aileen G Rowan and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
8.1field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

89 citing papers in PubMed, 141 citations in OpenAlex.

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  11. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
    Review
  12. Review
  13. Article
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  15. Article
  16. Viral remodeling of the 4D nucleome.Experimental & molecular medicine · 2024
    Review
  17. Article
  18. Review
  19. The Pleiotropic Effects of YBX1 on HTLV-1 Transcription.International journal of molecular sciences · 2023
    Article
  20. Article

29 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Yorifumi SatouSection of Virology, Division of Infectious Diseases, Imperial College, London W2 1PG, United Kingdom; Centre for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan; Priority Organization for Innovation and Excellence, Kumamoto University, Kumamoto 860-0811, Japan; International Research Centre for Medical Science, Kumamoto University, Kumamoto 860-0811, Japan; Core Research for Evolutionary Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan; c.bangham@imperial.ac.uk y-satou@kumamoto-u.ac.jp.
Paola MiyazatoCentre for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan; Priority Organization for Innovation and Excellence, Kumamoto University, Kumamoto 860-0811, Japan; International Research Centre for Medical Science, Kumamoto University, Kumamoto 860-0811, Japan;
Ko IshiharaPriority Organization for Innovation and Excellence, Kumamoto University, Kumamoto 860-0811, Japan; Core Research for Evolutionary Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan;
Hiroko YaguchiSection of Virology, Division of Infectious Diseases, Imperial College, London W2 1PG, United Kingdom;
Anat MelamedSection of Virology, Division of Infectious Diseases, Imperial College, London W2 1PG, United Kingdom;
Michi MiuraSection of Virology, Division of Infectious Diseases, Imperial College, London W2 1PG, United Kingdom;
Asami FukudaCentre for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan; Priority Organization for Innovation and Excellence, Kumamoto University, Kumamoto 860-0811, Japan; International Research Centre for Medical Science, Kumamoto University, Kumamoto 860-0811, Japan;
Kisato NosakaCancer Centre, Kumamoto University Hospital, Kumamoto University, Kumamoto 860-0811, Japan;
Takehisa WatanabeDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Aileen G RowanSection of Virology, Division of Infectious Diseases, Imperial College, London W2 1PG, United Kingdom;
Mitsuyoshi NakaoCore Research for Evolutionary Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan; Department of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Charles R M BanghamSection of Virology, Division of Infectious Diseases, Imperial College, London W2 1PG, United Kingdom; c.bangham@imperial.ac.uk y-satou@kumamoto-u.ac.jp.ORCID http://orcid.org/0000-0003-2624-3599
Imperial College London · GBJapan Science and Technology Agency · JPKumamoto University · JPKumamoto University Hospital · JP

Funding

Medical Research Council MR/K019090/1Wellcome Trust
6 · The paper itself

Abstract

Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that causes malignant and inflammatory diseases in ∼10% of infected people. A typical host has between 10(4) and 10(5) clones of HTLV-1-infected T lymphocytes, each clone distinguished by the genomic integration site of the single-copy HTLV-1 provirus. The HTLV-1 bZIP (HBZ) factor gene is constitutively expressed from the minus strand of the provirus, whereas plus-strand expression, required for viral propagation to uninfected cells, is suppressed or intermittent in vivo, allowing escape from host immune surveillance. It remains unknown what regulates this pattern of proviral transcription and latency. Here, we show that CTCF, a key regulator of chromatin structure and function, binds to the provirus at a sharp border in epigenetic modifications in the pX region of the HTLV-1 provirus in T cells naturally infected with HTLV-1. CTCF is a zinc-finger protein that binds to an insulator region in genomic DNA and plays a fundamental role in controlling higher order chromatin structure and gene expression in vertebrate cells. We show that CTCF bound to HTLV-1 acts as an enhancer blocker, regulates HTLV-1 mRNA splicing, and forms long-distance interactions with flanking host chromatin. CTCF-binding sites (CTCF-BSs) have been propagated throughout the genome by transposons in certain primate lineages, but CTCF binding has not previously been described in present-day exogenous retroviruses. The presence of an ectopic CTCF-BS introduced by the retrovirus in tens of thousands of genomic locations has the potential to cause widespread abnormalities in host cell chromatin structure and gene expression.

Indexed as

Epigenesis, GeneticGenome, HumanBasic-Leucine Zipper Transcription FactorsBinding SitesCCCTC-Binding FactorCD4-Positive T-LymphocytesChromatinChromatin ImmunoprecipitationConsensus SequenceDNADNA MethylationDNA, ViralGene Expression Regulation, ViralHistone CodeHTLV-I InfectionsHumansBasic-Leucine Zipper Transcription FactorsCCCTC-Binding FactorChromatinCTCF protein, humanDNADNA, ViralHBZ protein, human T-cell leukemia virus type IpX protein, Human T-lymphotropic virus 1Repressor ProteinsRetroviridae ProteinsTranscription FactorsViral Regulatory and Accessory ProteinsCTCFepigeneticsHTLV-1latencyretrovirus

Identifiers

PMID26929370
PMCPMC4801255
OpenAlexW2291064854

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.