ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Host factor transcriptional regulation contributes to preferential expression of HIV type 1 in IL-4-producing CD4 T cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 22 citations in OpenAlex.
- Single-cell characterization of the gastrointestinal HIV reservoir reveals heterogeneous cellular phenotypes.The Journal of clinical investigation · 2026Article
- Role of DOCK8 in cytokine storm syndromes.The Journal of allergy and clinical immunology · 2025Article
- HIV efficiently infects T cells from the endometrium and remodels them to promote systemic viral spread.eLife · 2020Article
- Methamphetamine functions as a novel CD4Scientific reports · 2019Article
- HIV-1 and Compromised Adult Neurogenesis: Emerging Evidence for a New Paradigm of HAND PersistenceAIDS reviews · 2019Review
- CD4AIDS research and human retroviruses · 2018Review
- Brief Report: Novel UNC13D Intronic Variant Disrupting an NF-κB Enhancer in a Patient With Recurrent Macrophage Activation Syndrome and Systemic Juvenile Idiopathic Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2018Article
- Regulatory CD4 T cells inhibit HIV-1 expression of other CD4 T cell subsets via interactions with cell surface regulatory proteins.Virology · 2018Article
- Clonal expansion of genome-intact HIV-1 in functionally polarized Th1 CD4+ T cells.The Journal of clinical investigation · 2017Article
- Functional Incompatibility between the Generic NF-κB Motif and a Subtype-Specific Sp1III Element Drives the Formation of the HIV-1 Subtype C Viral Promoter.Journal of virology · 2016Article
- Interference with nuclear factor kappaB signaling pathway by pathogen-encoded proteases: global and selective inhibition.Molecular microbiology · 2016Review
- HIV-1 latency and virus production from unintegrated genomes following direct infection of resting CD4 T cells.Retrovirology · 2016Article
- Blimp-1, an intrinsic factor that represses HIV-1 proviral transcription in memory CD4+ T cells.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- The impact of Nucleofection® on the activation state of primary human CD4 T cells.Journal of immunological methods · 2014Article
- Kinase control of latent HIV-1 infection: PIM-1 kinase as a major contributor to HIV-1 reactivation.Journal of virology · 2014Article
- Article
- T Cell Transcription Factors and Their Impact on HIV Expression.Virology : research and treatment · 2013Article
- Calcium/calcineurin synergizes with prostratin to promote NF-κB dependent activation of latent HIV.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
HIV type 1 (HIV-1) replicates preferentially in IL-4-producing CD4 T cells for unclear reasons. We show increased HIV-1 expression is irrespective of viral tropism for chemokine receptors as previously suggested, but rather transcription of the HIV-1 long terminal repeat (LTR) is increased in IL-4-producing CD4 T cells. Increased expression of HIV-1 message is also confirmed in IL-4-producing CD4 T cells from HIV-1-infected individuals ex vivo. In exploring a transcriptional mechanism, we identify a novel c-maf (required for IL-4 expression) transcription factor binding site just upstream of the dual NF-κB/NFAT binding sites in the proximal HIV-1 LTR. We demonstrate that c-maf binds this site in vivo and synergistically augments HIV-1 transcription in cooperation with NFAT2 and NF-κB p65, but not NFAT1 or NF-κB p50. Conversely, small interfering RNA inhibition of c-maf reduces HIV-1 transcription in IL-4-producing T cells. Thus, c-maf increases HIV-1 expression in IL-4-producing CD4 T cells by binding the proximal HIV-1 LTR and augmenting HIV-1 transcription in partnership with NFAT2 and NF-κB p65 specifically. This has important implications for selective targeting of transcription factors during HIV-1 infection because, over the course of HIV-1 progression/AIDS, IL-4-producing T cells frequently predominate and substantially contribute to disease pathology.
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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.