ArticlePloS one2011
The AP-1 binding sites located in the pol gene intragenic regulatory region of HIV-1 are important for viral replication.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 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
- Atlas of HIV cis-regulatory elements reveals extensive transcriptional variation across clades, isolates, and within individuals.bioRxiv : the preprint server for biology · 2026Article
- The KT Jeang retrovirology prize 2025: Carine Van Lint.Retrovirology · 2026Article
- Review
- The cellular activating protein-1 cFos regulates influenza A virus replication.The Journal of general virology · 2026Article
- Intra-pol proviral open region of HTLV-1 controls the transcription from both long terminal repeats.Retrovirology · 2025Article
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- Review
- Novel role of UHRF1 in the epigenetic repression of the latent HIV-1.EBioMedicine · 2022Article
- The Regulation of Prototype Foamy Virus 5'Long Terminal Repeats and Internal Promoter by Endogenous Transcription Factors.Intervirology · 2022Article
- AP-1 and NF-κB synergize to transcriptionally activate latent HIV upon T-cell receptor activation.FEBS letters · 2021Article
- Review
- Chromatin maturation of the HIV-1 provirus in primary resting CD4+ T cells.PLoS pathogens · 2020Article
- Distinctive variation in the U3R region of the 5' Long Terminal Repeat from diverse HIV-1 strains.PloS one · 2018Article
- Opposite transcriptional regulation of integrated vs unintegrated HIV genomes by the NF-κB pathway.Scientific reports · 2016Article
- Convergent Transcription of Interferon-stimulated Genes by TNF-α and IFN-α Augments Antiviral Activity against HCV and HEV.Scientific reports · 2016Article
- Review
- HIV-1 transcription and latency: an update.Retrovirology · 2013Review
- Human serum protein enhances HIV-1 replication and up-regulates the transcription factor AP-1.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our laboratory has previously identified an important intragenic region in the human immunodeficiency virus type 1 (HIV-1) genome, whose complete functional unit is composed of the 5103 fragment, the DNaseI-hypersensitive site HS7 and the 5105 fragment. These fragments (5103 and 5105) both exhibit a phorbol 12-myristate 13-acetate (PMA)-inducible enhancer activity on the herpes simplex virus thymidine kinase promoter. Here, we characterized the three previously identified AP-1 binding sites of fragment 5103 by showing the PMA-inducible in vitro binding and in vivo recruitment of c-Fos, JunB and JunD to this fragment located at the end of the pol gene. Functional analyses demonstrated that the intragenic AP-1 binding sites are fully responsible for the PMA-dependent enhancer activity of fragment 5103. Moreover, infection of T-lymphoid Jurkat and promonocytic U937 cells with wild-type and mutant viruses demonstrated that mutations of the intragenic AP-1 sites individually or in combination altered HIV-1 replication. Importantly, mutations of the three intragenic AP-1 sites led to a decreased in vivo recruitment of RNA polymerase II to the viral promoter, strongly supporting that the deleterious effect of these mutations on viral replication occurs, at least partly, at the transcriptional level. Single-round infections of monocyte-derived macrophages confirmed the importance of intragenic AP-1 sites for HIV-1 infectivity.
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