Evidence map›Paper›PMID 25310595›Full record

ArticleVirology2014

Sulfonation pathway inhibitors block reactivation of latent HIV-1.

Jeffrey P Murry, Joseph Godoy, Amey Mukim, Justine Swann, James W Bruce, Paul Ahlquist, Alberto Bosque, Vicente Planelles, Celsa A Spina, John A T Young

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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. The Cultured TMethods in molecular biology (Clifton, N.J.) · 2022
    Article
  3. Article
  4. Review
  5. Article
  6. 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.

Jeffrey P MurryNomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd., La Jolla, CA 92037, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Joseph GodoyVeterans Affairs San Diego Healthcare System, San Diego, CA, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Amey MukimVeterans Affairs San Diego Healthcare System, San Diego, CA, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Justine SwannNomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd., La Jolla, CA 92037, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
James W BruceMorgridge Institute for Research, Madison, WI, USA; Institute for Molecular Virology, University of Wisconsin, Madison, WI, USA; McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Paul AhlquistMorgridge Institute for Research, Madison, WI, USA; Institute for Molecular Virology, University of Wisconsin, Madison, WI, USA; McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Alberto BosqueDepartment of Pathology, University of California, San Diego, La Jolla, CA, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Vicente PlanellesDepartment of Pathology, University of California, San Diego, La Jolla, CA, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Celsa A SpinaVeterans Affairs San Diego Healthcare System, San Diego, CA, USA; Department of Pathology, University of California, San Diego, La Jolla, CA, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
John A T YoungNomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd., La Jolla, CA 92037, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA. Electronic address: jyoung@salk.edu.

Funding

VirologyP30AI036214 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI David Mitchell Smith · 1994 to 2026
$78.4M
Visualizing EBV and HCMV DNA Dynamics During InfectionP01CA022443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Paul F. Lambert · 1985 to 2026
$53.1M
Using NK Cells to eliminate the latent HIV reservoirU19AI096113 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MARGOLIS, DAVID M. · 2011 to 2015
$39.5M
Cellular factors in gammaretrovirus replicationR01AI072645 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI YOUNG, JOHN A T · 2007 to 2011
$2.2M
Control of Latent/Persistent HIV Infection in Primary CD4 T CellsI01BX001160 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI SPINA, CELSA A · 2011 to 2014
–
BLRD VA I01 BX001160NCI NIH HHS P01 CA022443NIAID NIH HHS AI036214NIAID NIH HHS AI072645NIAID NIH HHS AI096113NIAID NIH HHS P30 AI036214NIAID NIH HHS R01 AI072645NIAID NIH HHS U19 AI096113
6 · The paper itself

Abstract

Long-lived pools of latently infected cells are a significant barrier to the development of a cure for HIV-1 infection. A better understanding of the mechanisms of reactivation from latency is needed to facilitate the development of novel therapies that address this problem. Here we show that chemical inhibitors of the sulfonation pathway prevent virus reactivation, both in latently infected J-Lat and U1 cell lines and in a primary human CD4+ T cell model of latency. In each of these models, sulfonation inhibitors decreased transcription initiation from the HIV-1 promoter. These inhibitors block transcription initiation at a step that lies downstream of nucleosome remodeling and affects RNA polymerase II recruitment to the viral promoter. These results suggest that the sulfonation pathway acts by a novel mechanism to regulate efficient virus transcription initiation during reactivation from latency, and further that augmentation of this pathway could be therapeutically useful.

Indexed as

Anti-HIV AgentsCD4-Positive T-LymphocytesCell LineChloratesDrug Therapy, CombinationGene Expression Regulation, ViralGuaiacolHIV-1HIV Long Terminal RepeatHumansNF-kappa BRNA Polymerase IISulfonic AcidsTumor Necrosis Factor-alphaVirus ActivationVirus LatencyAnti-HIV AgentsChloratesGuaiacolNF-kappa BRNA Polymerase IISulfonic AcidsTumor Necrosis Factor-alphaGene expressionHIV-1InhibitorLatencyPrimary CD4+ T cellsReactivationSulfonation

Identifiers

PMID25310595
PMCPMC4392775

What OpenQuestion holds

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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.