ArticleScientific reports2016
Opposite transcriptional regulation of integrated vs unintegrated HIV genomes by the NF-κB pathway.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Effect of TAR hairpin stabilization on HIV-1 reverse transcription.Journal of virology · 2026Article
- High-resolution HIV-1 mNAR genomics and bioinformatics · 2025Article
- Reverse transcription of HIV-1 2-LTR circle transcripts does frequently cause 3'-polypurine tract mutations implicated in dolutegravir resistance.Journal of virology · 2024Article
- HIV-1 3'-Polypurine Tract Mutations Confer Dolutegravir Resistance by Switching to an Integration-Independent Replication Mechanism via 1-LTR Circles.Journal of virology · 2023Article
- Article
- Epigenetic Mechanisms of HIV-1 Persistence.Vaccines · 2021Review
- Distribution and fate of HIV-1 unintegrated DNA species: a comprehensive update.AIDS research and therapy · 2017Review
- A systematic comparison reveals substantial differences in chromosomal versus episomal encoding of enhancer activity.Genome research · 2017Article
- Total HIV-1 DNA, a Marker of Viral Reservoir Dynamics with Clinical Implications.Clinical microbiology reviews · 2016Review
- Different Pathways Leading to Integrase Inhibitors Resistance.Frontiers in microbiology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Integration of HIV-1 linear DNA into host chromatin is required for high levels of viral expression, and constitutes a key therapeutic target. Unintegrated viral DNA (uDNA) can support only limited transcription but may contribute to viral propagation, persistence and/or treatment escape under specific situations. The molecular mechanisms involved in the differential expression of HIV uDNA vs integrated genome (iDNA) remain to be elucidated. Here, we demonstrate, for the first time, that the expression of HIV uDNA is mainly supported by 1-LTR circles, and regulated in the opposite way, relatively to iDNA, following NF-κB pathway modulation. Upon treatment activating the NF-κB pathway, NF-κB p65 and AP-1 (cFos/cJun) binding to HIV LTR iDNA correlates with increased iDNA expression, while uDNA expression decreases. On the contrary, inhibition of the NF-κB pathway promotes the expression of circular uDNA, and correlates with Bcl-3 and AP-1 binding to its LTR region. Finally, this study identifies NF-κB subunits and Bcl-3 as transcription factors binding the HIV promoter differently depending on viral genome topology, and opens new insights on the potential roles of episomal genomes during the HIV-1 latency and persistence.
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Registered trials
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