Evidence map›Paper›PMID 31999790›Full record

ArticlePLoS pathogens2020

Chromatin maturation of the HIV-1 provirus in primary resting CD4+ T cells.

Birgitta Lindqvist, Sara Svensson Akusjärvi, Anders Sönnerborg, Marios Dimitriou, J Peter Svensson

Abstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Review
  2. Traditional Medicine Extracts ofInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Effective and targeted latency reversal in CD4Emerging microbes & infections · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Targeting Epigenetics to Cure HIV-1: Lessons From (and for) Cancer Treatment.Frontiers in cellular and infection microbiology · 2021
    Review
  20. Article
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

5 authors.

Birgitta LindqvistDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Sara Svensson AkusjärviDivision of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0002-1086-5409
Anders SönnerborgDivision of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0001-8928-3374
Marios DimitriouDepartment of Medicine Huddinge, Center for Hematology and Regenerative Medicine, Karolinska Institutet, Huddinge, Sweden.
J Peter SvenssonDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0002-5863-6250

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) infection is a chronic condition, where viral DNA integrates into the genome. Latently infected cells form a persistent, heterogeneous reservoir that at any time can reactivate the integrated HIV-1. Here we confirmed that latently infected cells from HIV-1 positive study participants exhibited active HIV-1 transcription but without production of mature spliced mRNAs. To elucidate the mechanisms behind this we employed primary HIV-1 latency models to study latency establishment and maintenance. We characterized proviral transcription and chromatin development in cultures of resting primary CD4+ T-cells for four months after ex vivo HIV-1 infection. As heterochromatin (marked with H3K9me3 or H3K27me3) gradually stabilized, the provirus became less accessible with reduced activation potential. In a subset of infected cells, active marks (e.g. H3K27ac) and elongating RNAPII remained detectable at the latent provirus, despite prolonged proviral silencing. In many aspects, latent HIV-1 resembled an active enhancer in a subset of resting cells. The enhancer chromatin actively promoted latency and the enhancer-specific CBP/P300-inhibitor GNE049 was identified as a new latency reversal agent. The division of the latent reservoir according to distinct chromatin compositions with different reactivation potential enforces the notion that even though a relatively large set of cells contains the HIV-1 provirus, only a discrete subset is readily able to reactivate the provirus and spread the infection.

Indexed as

CD4-Positive T-LymphocytesChromatinHIV-1HIV InfectionsHumansProvirusesVirus ActivationVirus AssemblyVirus LatencyChromatin

Identifiers

PMID31999790
PMCPMC6991963

What OpenQuestion holds

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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.