Evidence map›Paper›PMID 9371597›Full record

ArticleJournal of virology1997

Repression of human immunodeficiency virus type 1 through the novel cooperation of human factors YY1 and LSF.

F Romerio, M N Gabriel, D M Margolis

Erratum issued Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT02707900 (IGHID 11424 - A Pilot Trial of the Effect of Vorinostat and AGS-004 on Persistent HIV-1 Infection), which is not on this map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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.

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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
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  9. Article
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  11. Review
  12. SUMOylation-mediated PSME3-20Science advances · 2023
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Insights into the HIV Latency and the Role of Cytokines.Pathogens (Basel, Switzerland) · 2019
    Review
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

F RomerioInstitute of Human Virology, Medical Biotechnology Center, University of Maryland Biotechnology Institute, Baltimore 21201, USA.
M N Gabriel
D M Margolis
Biotechnology Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A subpopulation of stably infected CD4+ cells capable of producing virus upon stimulation has been identified in human immunodeficiency virus (HIV)-positive individuals (T.-W. Chun, D. Finzi, J. Margolick, K. Chadwick, D. Schwartz, and R. F. Siliciano, Nat. Med. 1:1284-1290, 1995). Few host factors that directly limit HIV-1 transcription and could support this state of nonproductive HIV-1 infection have been described. YY1, a widely distributed human transcription factor, is known to inhibit HIV-1 long terminal repeat (LTR) transcription and virus production. LSF (also known as LBP-1, UBP, and CP-2) has been shown to repress LTR transcription in vitro, but transient expression of LSF has no effect on LTR activity in vivo. We report that both YY1 and LSF participate in the formation of a complex that recognizes the initiation region of the HIV-1 LTR. Further, we have found that these factors cooperate in the repression of LTR expression and viral replication. This cooperative function may account for the divergent effects of LSF previously observed in vitro and in vivo. Thus, the cooperation of two general cellular transcription factors may allow for the selective downregulation of HIV transcription. Through this mechanism of gene regulation, YY1 and LSF could contribute to the establishment and maintenance of a population of cells stably but nonproductively infected with HIV-1.

Indexed as

Gene Expression Regulation, ViralHIV Long Terminal RepeatCell LineDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsHIV-1HumansLymphocytesMonocytesMutationRepressor ProteinsRNA-Binding ProteinsTranscription FactorsYY1 Transcription FactorDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsRepressor ProteinsRNA-Binding ProteinsTFCP2 protein, humanTranscription FactorsYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID9371597
PMCPMC230241
OpenAlexW2139996002

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.