Evidence map›Paper›PMID 21228324›Full record

ArticleBlood2011

The host genomic environment of the provirus determines the abundance of HTLV-1-infected T-cell clones.

Nicolas A Gillet, Nirav Malani, Anat Melamed, Niall Gormley, Richard Carter, David Bentley, Charles Berry, Frederic D Bushman, Graham P Taylor, Charles R M Bangham

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed
8.8field-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

207 citing papers in PubMed, 320 citations in OpenAlex.

  1. Clinical trial of raltegravir, an integrase inhibitor, in HAM/TSP.Annals of clinical and translational neurology · 2021
    Trial
  2. Trial
  3. Article
  4. Loss of HTLV-1-specific CD8Blood neoplasia · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Case report:Frontiers in oncology · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

147 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

10 authors at 4 institutions in 2 countries.

Nicolas A GilletDepartment of Immunology, Wright-Fleming Institute, Imperial College London, London, UK. n.gillet@ulg.ac.be
Nirav Malani
Anat Melamed
Niall Gormley
Richard Carter
David Bentley
Charles Berry
Frederic D Bushman
Graham P Taylor
Charles R M Bangham
Imperial College London · GBIllumina (United Kingdom) · GBUniversity of Pennsylvania · USUniversity of California, San Diego · US

Funding

Favored Sites for HIV Integration in the Human GenomeR01AI052845 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI BUSHMAN, FREDERIC D · 2002 to 2017
$5.6M
NIAID NIH HHS R01 AI052845Wellcome Trust
6 · The paper itself

Abstract

Human T-lymphotropic virus type 1 (HTLV-1) persists by driving clonal proliferation of infected T lymphocytes. A high proviral load predisposes to HTLV-1-associated diseases. Yet the reasons for the variation within and between persons in the abundance of HTLV-1-infected clones remain unknown. We devised a high-throughput protocol to map the genomic location and quantify the abundance of > 91,000 unique insertion sites of the provirus from 61 HTLV-1(+) persons and > 2100 sites from in vitro infection. We show that a typical HTLV-1-infected host carries between 500 and 5000 unique insertion sites. We demonstrate that negative selection dominates during chronic infection, favoring establishment of proviruses integrated in transcriptionally silenced DNA: this selection is significantly stronger in asymptomatic carriers. We define a parameter, the oligoclonality index, to quantify clonality. The high proviral load characteristic of HTLV-1-associated inflammatory disease results from a larger number of unique insertion sites than in asymptomatic carriers and not, as previously thought, from a difference in clonality. The abundance of established HTLV-1 clones is determined by genomic features of the host DNA flanking the provirus. HTLV-1 clonal expansion in vivo is favored by orientation of the provirus in the same sense as the nearest host gene.

Indexed as

Cell ProliferationClone CellsEpigenesis, GeneticGenome, HumanHost-Pathogen InteractionsHTLV-I InfectionsHumansHuman T-lymphotropic virus 1Middle AgedMutagenesis, InsertionalPolymerase Chain ReactionProvirusesTime FactorsT-LymphocytesTranscription, GeneticVirus Integration

Identifiers

PMID21228324
PMCPMC3062313
OpenAlexW2043248836

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.