Evidence map›Paper›PMID 24418551›Full record

ArticleVirology2014

Epigenetic analysis of HIV-1 proviral genomes from infected individuals: predominance of unmethylated CpG's.

Stefanie Weber, Barbara Weiser, Kimdar S Kemal, Harold Burger, Christina M Ramirez, Klaus Korn, Kathryn Anastos, Rupert Kaul, Colin Kovacs, Walter Doerfler

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Tuning Rex rules HTLV-1 pathogenesis.Frontiers in immunology · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Deciphering DNA Methylation in HIV Infection.Frontiers in immunology · 2021
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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.

Stefanie WeberInstitute for Clinical and Molecular Virology, Erlangen University Medical School, Schlossgarten 4, D-91054 Erlangen, Germany.
Barbara WeiserUniversity of California, Davis School of Medicine and Sacramento Veterans Administration Medical Center, Sacramento, CA 95655, USA.
Kimdar S KemalAlbert Einstein College of Medicine, Bronx, NY 10461, USA.
Harold BurgerUniversity of California, Davis School of Medicine and Sacramento Veterans Administration Medical Center, Sacramento, CA 95655, USA.
Christina M RamirezUniversity of California, Los Angeles, CA 90095, USA.
Klaus KornInstitute for Clinical and Molecular Virology, Erlangen University Medical School, Schlossgarten 4, D-91054 Erlangen, Germany.
Kathryn AnastosAlbert Einstein College of Medicine, Bronx, NY 10461, USA.
Rupert KaulUniversity of Toronto, Toronto, ON, Canada M55 1A8.
Colin KovacsUniversity of Toronto, Toronto, ON, Canada M55 1A8.
Walter DoerflerInstitute for Clinical and Molecular Virology, Erlangen University Medical School, Schlossgarten 4, D-91054 Erlangen, Germany; Institute of Genetics, University of Cologne, D-50674 Cologne, Germany. Electronic address: walter.doerfler@viro.med.uni-erlangen.de.

Funding

Women's Interagency HIV Study (WIHS-V)U01AI035004 · NIAID · MONTEFIORE MEDICAL CENTER (BRONX, NY) · PI ANASTOS, KATHRYN M., SHARMA, ANJALI · 1993 to 2018
$65.7M
CIHR HET-85518NIAID NIH HHS U01 AI035004NIAID NIH HHS UO1-AI35004
6 · The paper itself

Abstract

Efforts to cure HIV-1 infections aim at eliminating proviral DNA. Integrated DNA from various viruses often becomes methylated de novo and transcriptionally inactivated. We therefore investigated CpG methylation profiles of 55 of 94 CpG's (58.5%) in HIV-1 proviral genomes including ten CpG's in each LTR and additional CpG's in portions of gag, env, nef, rev, and tat genes. We analyzed 33 DNA samples from PBMC's of 23 subjects representing a broad spectrum of HIV-1 disease. In 22 of 23 HIV-1-infected individuals, there were only unmethylated CpG's regardless of infection status. In one long term nonprogressor, however, methylation of proviral DNA varied between 0 and 75% over an 11-year period although the CD4+ counts remained stable. Hence levels of proviral DNA methylation can fluctuate. The preponderance of unmethylated CpG's suggests that proviral methylation is not a major factor in regulating HIV-1 proviral activity in PBMC's. Unmethylated CpG's may play a role in HIV-1 immunopathogenesis.

Indexed as

Epigenesis, GeneticGenome, ViralAdultCells, CulturedDinucleoside PhosphatesDNA MethylationFemaleHIV-1HIV InfectionsHumansLeukocytes, MononuclearMaleProvirusesYoung AdultCpG dinucleotideDinucleoside PhosphatesBisulfite sequencingEpigenetics of HIV-1 proviral DNAEscape from proviral DNA methylationFluctuation of CpG methylation in one LTNP individualIntegrated HIV-1 DNA in PBMC's from infected individualsMethylation analysis of integrated HIV-1 genomesPredominance of unmethylated CpG's in PBMC'sWide spectrum of infection outcome

Identifiers

PMID24418551
PMCPMC4060985

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Registered trials

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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.