Evidence map›Paper›PMID 26852322›Full record

ArticleRetrovirology2016

Human endogenous retrovirus (HERV) expression is not induced by treatment with the histone deacetylase (HDAC) inhibitors in cellular models of HIV-1 latency.

Tara Hurst, Matthew Pace, Aris Katzourakis, Rodney Phillips, Paul Klenerman, John Frater, Gkikas Magiorkinis

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Human endogenous retroviruses and exogenous viral infections.Frontiers in cellular and infection microbiology · 2024
    Review
  5. Article
  6. Human Endogenous Retroviruses in Diseases.Sub-cellular biochemistry · 2023
    Article
  7. Retroviral Elements in Pathophysiology and as Therapeutic Targets for Amyotrophic Lateral Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
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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

7 authors at 3 institutions in 1 country.

Tara HurstDepartment of Zoology, University of Oxford, South Parks Road, Oxford, UK. tara.hurst@zoo.ox.ac.uk.
Matthew PaceNuffield Department of Clinical Medicine, Peter Medawar Building for Pathogen Research, John Radcliffe Hospital, Oxford, UK. matthew.pace@ndm.ox.ac.uk.
Aris KatzourakisDepartment of Zoology, University of Oxford, South Parks Road, Oxford, UK. aris.katzourakis@zoo.ox.ac.uk.
Rodney PhillipsNuffield Department of Clinical Medicine, Peter Medawar Building for Pathogen Research, John Radcliffe Hospital, Oxford, UK. rodney.phillips@unsw.edu.au.
Paul KlenermanNuffield Department of Clinical Medicine, Peter Medawar Building for Pathogen Research, John Radcliffe Hospital, Oxford, UK. paul.klenerman@medawar.ox.ac.uk.
John FraterNuffield Department of Clinical Medicine, Peter Medawar Building for Pathogen Research, John Radcliffe Hospital, Oxford, UK. john.frater@ndm.ox.ac.uk.
Gkikas MagiorkinisDepartment of Zoology, University of Oxford, South Parks Road, Oxford, UK. gkikas.magiorkinis@zoo.ox.ac.uk.
Medawar Building for Pathogen Research · GBUniversity of Oxford · GBJohn Radcliffe Hospital · GB

Funding

Medical Research Council MR/L006588/1Wellcome Trust 091663Wellcome Trust 109965/Z/15/Z
6 · The paper itself

Abstract

backgroundWhile antiretroviral therapies have improved life expectancy and reduced viral loads in HIV-1-positive individuals, the cessation of treatment results in a rebound of viral replication. This suggests that a reservoir of latently-infected cells remains within these patients, the identity of which is ill-defined and therefore difficult to target therapeutically. Current strategies are aimed at using drugs such as histone deacetylase (HDAC) inhibitors to induce the expression of latent HIV-1 proviruses in order to activate and ultimately eradicate this reservoir of infected cells. One concern with the use of HDAC inhibitors is that they could up-regulate human endogenous retroviruses (HERVs), as well as HIV-1, with potentially pathophysiological consequences.

resultsIn this study, we analysed the transcription of HERV genes in HIV-1 latency T cell (J-LAT 8.4) and monocyte (U1) models following treatment with the HDAC inhibitors, vorinostat, panobinostat and romidepsin. We examined the expression of HERV-K (HML-2) env and pol, as well as the co-opted genes HERV-W env (syncytin-1), HERV-FRD env (syncytin-2), in these cell lines. Finally, we investigated HERV expression in primary human T cells.

conclusionsWe show that HDAC inhibitors did not substantially increase the transcription of the analysed HERV env or pol genes, suggesting that histone acetylation is not crucial for controlling HERV expression in these experimental models and in ex vivo primary human T cells. Importantly, this indicates that unwanted HERV expression does not appear to be a barrier to the use of HDAC inhibitors in HIV-1 cure strategies.

Indexed as

Cell LineEndogenous RetrovirusesGene Products, envGene Products, polHistone Deacetylase InhibitorsHIV-1HumansMonocytesProvirusesT-LymphocytesTranscription, GeneticVirus ActivationGene Products, envGene Products, polHistone Deacetylase Inhibitors

Identifiers

PMID26852322
PMCPMC4744380
OpenAlexW2286216483

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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.