ReviewGene expression1999
Regulation of HIV-1 transcription.
Review in Gene expression, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Computationally inferred cell-type specific epigenome-wide DNA methylation analysis unveils distinct methylation patterns among immune cells for HIV infection in three cohorts.PLoS pathogens · 2024Pooled it
- 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
- HIV-1-encoded circular RNA enhances viral transcription through Tat binding.Nature microbiology · 2026Article
- Molecular Investigation of Product Nkabinde in HIV Therapy: A Network Pharmacology and Molecular Docking Approach.International journal of molecular sciences · 2026Article
- Integrative genomic and immunoinformatic approach for characterizing HIV-1 pol, vpr, and Nef genes and designing a multi-epitope vaccine.Scientific reports · 2025Article
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- The role of Tat in HIV latency and reactivation.Frontiers in immunology · 2025Review
- NSC95397 Is a Novel HIV-1 Latency-Reversing Agent.Viruses · 2024Article
- NSC95397 is a Novel HIV-1 Latency Reversing Agent.bioRxiv : the preprint server for biology · 2024Article
- Review
- Kinetic pathway of HIV-1 TAR cotranscriptional folding.Nucleic acids research · 2024Article
- Structural elucidation of HIV-1 G-quadruplexes in a cellular environment and their ligand binding using responsiveChemical science · 2024Article
- Integrated Single-cell Multiomic Analysis of HIV Latency Reversal Reveals Novel Regulators of Viral Reactivation.Genomics, proteomics & bioinformatics · 2024Article
- Bioinformatics Insights on Viral Gene Expression Transactivation: From HIV-1 to SARS-CoV-2.International journal of molecular sciences · 2024Article
- HIV Expression in Infected T Cell Clones.Viruses · 2024Review
- Breaking the Silence: Regulation of HIV Transcription and Latency on the Road to a Cure.Viruses · 2023Review
- The role of tunneling nanotubes during early stages of HIV infection and reactivation: implications in HIV cure.NeuroImmune pharmacology and therapeutics · 2023Review
- HIV-Host Cell Interactions.Cells · 2023Review
- Analysis of regulatory sequences in exosomal DNA of NANOGP8.PloS one · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus type-1 (HIV-1) is a highly pathogenic lentivirus that requires transcription of its provirus genome for completion of the viral life cycle and the production of progeny virions. Since the first genetic analysis of HIV-1 in 1985, much has been learned about the transcriptional regulation of the HIV-1 genome in infected cells. It has been demonstrated that HIV-1 transcription depends on a varied and complex interaction of host cell transcription factors with the viral long terminal repeat (LTR) promoter. The regulatory elements within the LTR interact with constitutive and inducible transcription factors to direct the assembly of a stable transcription complex that stimulates multiple rounds of transcription by RNA polymerase II (RNAPII). However, the majority of these transcripts terminate prematurely in the absence of the virally encoded trans-activator protein Tat, which stimulates HIV-1 transcription elongation by interacting with a stem-loop RNA element (TAR) formed at the extreme 5' end of all viral transcripts. The Tat-TAR interaction recruits a cellular kinase into the initiation-elongation complex that alters the elongation properties of RNAPII during its transit through TAR. This review summarizes our current knowledge and understanding of the regulation of HIV-1 transcription in infected cells and highlights the important contributions human lentivirus gene regulation has made to our general understanding of the transcription process.
Indexed as
Identifiers
10551796PMC6157391W2425917325What OpenQuestion holds
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.