ArticleJournal of virology2003
Transcriptional suppression of in vitro-integrated human immunodeficiency virus type 1 does not correlate with proviral DNA methylation.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- Breaking into HIV-1's Epigenetic Vault: Cure Strategies to Eliminate the Viral Reservoir.Viruses · 2026Review
- HIV-Tocky system to visualize proviral expression dynamics.Communications biology · 2024Article
- Inhibition of the H3K27 demethylase UTX enhances the epigenetic silencing of HIV proviruses and induces HIV-1 DNA hypermethylation but fails to permanently block HIV reactivation.PLoS pathogens · 2021Article
- Balance between Retroviral Latency and Transcription: Based on HIV Model.Pathogens (Basel, Switzerland) · 2020Review
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- Longitudinal variation in human immunodeficiency virus long terminal repeat methylation in individuals on suppressive antiretroviral therapy.Clinical epigenetics · 2019Article
- HIV latency in isolated patient CD4Science translational medicine · 2018Article
- Combinations of isoform-targeted histone deacetylase inhibitors and bryostatin analogues display remarkable potency to activate latent HIV without global T-cell activation.Scientific reports · 2017Article
- Specific and Stable Suppression of HIV Provirus Expression In Vitro by Chimeric Zinc Finger DNA Methyltransferase 1.Molecular therapy. Nucleic acids · 2017Article
- Development of 5' LTR DNA methylation of latent HIV-1 provirus in cell line models and in long-term-infected individuals.Clinical epigenetics · 2016Article
- Designed transcription activator-like effector proteins efficiently induced the expression of latent HIV-1 in latently infected cells.AIDS research and human retroviruses · 2015Article
- Epigenetic analysis of HIV-1 proviral genomes from infected individuals: predominance of unmethylated CpG's.Virology · 2014Article
- HIV-1 transcription and latency: an update.Retrovirology · 2013Review
- Targeting IκB proteins for HIV latency activation: the role of individual IκB and NF-κB proteins.Journal of virology · 2013Article
- An AP-1 binding site in the enhancer/core element of the HIV-1 promoter controls the ability of HIV-1 to establish latent infection.Journal of virology · 2013Article
- Selected drugs with reported secondary cell-differentiating capacity prime latent HIV-1 infection for reactivation.Journal of virology · 2012Article
- Achieving a cure for HIV infection: do we have reasons to be optimistic?The Journal of antimicrobial chemotherapy · 2012Review
- Combination of biological screening in a cellular model of viral latency and virtual screening identifies novel compounds that reactivate HIV-1.Journal of virology · 2012Article
- Innate and adaptive factors regulating human immunodeficiency virus type 1 genomic activation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Review
- Establishment of HIV latency in primary CD4+ cells is due to epigenetic transcriptional silencing and P-TEFb restriction.Journal of virology · 2010Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistence of human immunodeficiency virus type 1 (HIV-1) constitutes a major obstacle in the control of HIV-1 infection. Here we investigated whether the CpG methylation of the HIV-1 promoter can directly influence the expression of the HIV-1 genome and thereby contribute to the persistence and latency of HIV-1. The levels of CpG methylation in the promoter of HIV-1 were studied after bisulfite-induced modification of DNA in five Jurkat clonal cell lines transduced by an HIV-1 long terminal repeat (LTR)-driven retroviral vector and expressing enhanced green fluorescent protein (GFP) and in primary resting memory T cells challenged with HIV-1 or with an HIV-1-derived retroviral vector. Basal HIV-1 promoter activities were low or undetectable in three tested HIV-1 LTR-GFP clones, one of which encoded the Tat protein, and they reached medium or high levels in two other clones. The CpG dinucleotide that occurred in a latently infected clonal cell line 240 nucleotides upstream of the transcription start remained methylated after reactivation of HIV-1 transcription with 10 nM phorbol-12-myristate-13-acetate. In two clones showing a medium promoter activity and in resting memory T cells, the HIV-1 LTR was generally not methylated. Our results show that the methylation profiles of the HIV-1 LTR, including those present in latently infected cells, are low and do not correlate with the transcriptional activity. We suggest that, in a noncloned cellular population in which the HIV-1 proviruses are randomly integrated in the human genome, HIV-1 latency is imperfectly controlled by CpG methylation and is inherently accompanied by residual replication.
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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.