ArticlePLoS pathogens2021
Epigenomic characterization of latent HIV infection identifies latency regulating transcription factors.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Identification of the cellular factor KLF16 as a novel epigenetic repressor of HIV-1 transcription.Research square · 2026Article
- Identification of the cellular transcription factor KLF16 as a novel repressive epigenetic repressor of HIV-1 transcription.bioRxiv : the preprint server for biology · 2026Article
- Single cell multiomic analysis of the impact of Delta-9-tetrahydrocannabinol on HIV infected CD4 T cells.Journal of cannabis research · 2026Article
- Traditional Medicine Extracts ofInternational journal of molecular sciences · 2026Article
- Review
- Maladaptive trained immunity in viral infections.The Journal of clinical investigation · 2025Review
- Using single cell technologies to understand HIV latency models.Current opinion in HIV and AIDS · 2025Review
- HIV-1 accessory protein Vpr possesses a cryptic p300-dependent transcription-promoting activity that is blocked by histone deacetylases in CD4+ T cells.PLoS pathogens · 2025Article
- Advancements in single-cell techniques for examining the HIV reservoir: pathways to a cure.mBio · 2025Review
- Suppression of HIV-1 transcription and latency reversal via ectopic expression of the viral antisense transcript AST.Science advances · 2025Article
- A targeted CRISPR screen identifies ETS1 as a regulator of HIV-1 latency.PLoS pathogens · 2025Article
- Impact of chromatin on HIV-1 latency: a multi-dimensional perspective.Epigenetics & chromatin · 2025Review
- Aberrant DNA methylation of genes regulating CD4+ T cell HIV-1 reservoir in women with HIV.Clinical and translational medicine · 2025Article
- Comprehensive SUMO Proteomic Analyses Identify HIV Latency-Associated Proteins in Microglia.Cells · 2025Article
- The role of Tat in HIV latency and reactivation.Frontiers in immunology · 2025Review
- The histone methyltransferase SETD2 regulates HIV expression and latency.PLoS pathogens · 2024Article
- Integrated Single-cell Multiomic Analysis of HIV Latency Reversal Reveals Novel Regulators of Viral Reactivation.Genomics, proteomics & bioinformatics · 2024Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- Viral remodeling of the 4D nucleome.Experimental & molecular medicine · 2024Review
- Primary T-cell-based delivery platform for in vivo synthesis of engineered proteins.Bioengineering & translational medicine · 2024Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Transcriptional silencing of HIV in CD4 T cells generates a reservoir of latently infected cells that can reseed infection after interruption of therapy. As such, these cells represent the principal barrier to curing HIV infection, but little is known about their characteristics. To further our understanding of the molecular mechanisms of latency, we characterized a primary cell model of HIV latency in which infected cells adopt heterogeneous transcriptional fates. In this model, we observed that latency is a stable, heritable state that is transmitted through cell division. Using Assay of Transposon-Accessible Chromatin sequencing (ATACseq) we found that latently infected cells exhibit greatly reduced proviral accessibility, indicating the presence of chromatin-based structural barriers to viral gene expression. By quantifying the activity of host cell transcription factors, we observe elevated activity of Forkhead and Kruppel-like factor transcription factors (TFs), and reduced activity of AP-1, RUNX and GATA TFs in latently infected cells. Interestingly, latency reversing agents with different mechanisms of action caused distinct patterns of chromatin reopening across the provirus. We observe that binding sites for the chromatin insulator CTCF are highly enriched in the differentially open chromatin of infected CD4 T cells. Furthermore, depletion of CTCF inhibited HIV latency, identifying this factor as playing a key role in the initiation or enforcement of latency. These data indicate that HIV latency develops preferentially in cells with a distinct pattern of TF activity that promotes a closed proviral structure and inhibits viral gene expression. Furthermore, these findings identify CTCF as a novel regulator of HIV latency.
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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.