Evidence map›Paper›PMID 17670825›Full record

ArticleJournal of virology2007

c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter.

Guochun Jiang, Amy Espeseth, Daria J Hazuda, David M Margolis

2 registry-linked trialsOpen access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 144 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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.

NCT00312546 phase1terminatednot on this map

Inhibiting Histone Deacetylase: Toward Eradication of HIV

TypeinterventionalSponsorUniversity of North Carolina, Chapel HillRan2006 to 2009Enrolled14ConditionsHIV InfectionsArmsEnfuvirtide, Valproic acid
NCT02707900 phase1terminatednot on this mapstarted 2016, after this paper: background citation

IGHID 11424 - A Pilot Trial of the Effect of Vorinostat and AGS-004 on Persistent HIV-1 Infection (The VOR VAX Study)

TypeinterventionalSponsorUniversity of North Carolina, Chapel HillRan2016 to 2018Enrolled6ConditionsHIV-1 InfectionArmsVorinostat, AGS-004
3 · Its place in the literature

Who cites it

144 citing papers in PubMed, 1 synthesis or guideline pooled it, 213 citations in OpenAlex.

  1. Pooled it
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  11. NSC95397 is a Novel HIV-1 Latency Reversing Agent.bioRxiv : the preprint server for biology · 2024
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84 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

4 authors at 2 institutions in 1 country.

Guochun JiangDepartment of Medicine, University of North Carolina at Chapel Hill, 3302 Michael Hooker Research Ctr., Chapel Hill, NC 27599-7435, USA.
Amy Espeseth
Daria J Hazuda
David M Margolis
United States Military Academy · USUniversity of North Carolina at Chapel Hill · US

Funding

Virology, Immunology, and Microbiology CoreP30AI050410 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAVID M. MARGOLIS · 2001 to 2026
$76.9M
REPRESSION OF HIV TRANSCRIPTION--A PATHWAY TO QUIESCENCER01AI045297 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MARGOLIS, DAVID M. · 1999 to 2006
$2.5M
Clearing Persistently HIV-Infected CD4+ T LymphocytesR01AI064074 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MARGOLIS, DAVID M. · 2005 to 2008
$2.1M
Repression of HIV Transcription: from mechanism to anti-latency therapiesR56AI045297 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MARGOLIS, DAVID M. · 2007 to 2007
$329k
NIAID NIH HHS AI45297NIAID NIH HHS AI64074NIAID NIH HHS P30 AI050410NIAID NIH HHS P30 AI50410NIAID NIH HHS R01 AI045297NIAID NIH HHS R01 AI064074NIAID NIH HHS R56 AI045297
6 · The paper itself

Abstract

Histone deacetylase (HDAC) inhibitors such as valproic acid (VPA) induce the expression of quiescent proviral human immunodeficiency virus type 1 (HIV-1) and may deplete proviral infection in vivo. To uncover novel molecular mechanisms that maintain HIV latency, we sought cellular mRNAs whose expression was diminished in resting CD4(+) T cells of HIV-1-infected patients exposed to VPA. c-Myc was prominent among genes markedly downregulated upon exposure to VPA. c-Myc expression repressed HIV-1 expression in chronically infected cell lines. Chromatin immunoprecipitation (ChIP) assays revealed that c-Myc and HDAC1 are coordinately resident at the HIV-1 long terminal repeat (LTR) promoter and absent from the promoter after VPA treatment in concert with histone acetylation, RNA polymerase II recruitment, and LTR expression. Sequential ChIP assays demonstrated that c-Myc, Sp1, and HDAC1 coexist in the same DNA-protein complex at the HIV promoter. Short hairpin RNA inhibition of c-Myc reduces both c-Myc and HDAC1 occupancy, blocks c-Myc repression of Tat activation, and increases LTR expression. These results expand the understanding of mechanisms that recruit HDAC and maintain the latency of HIV-1, suggesting novel therapeutic approaches against latent proviral HIV infection.

Indexed as

Promoter Regions, GeneticVirus LatencyDown-RegulationHistone Deacetylase 1Histone Deacetylase InhibitorsHistone DeacetylasesHIV-1HIV Long Terminal RepeatHumansProto-Oncogene Proteins c-mycSp1 Transcription FactorValproic AcidHDAC1 protein, humanHistone Deacetylase 1Histone Deacetylase InhibitorsHistone DeacetylasesMYC protein, humanProto-Oncogene Proteins c-mycSp1 Transcription FactorValproic Acid

Identifiers

PMID17670825
PMCPMC2045540
OpenAlexW2122745942

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.