ArticleJournal of virology1996
Human immunodeficiency virus type 1 long terminal repeat variants from 42 patients representing all stages of infection display a wide range of sequence polymorphism and transcription activity.
Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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.
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Who cites it
38 citing papers in PubMed, 81 citations in OpenAlex.
- A Canadian Survey of Research on HIV-1 Latency-Where Are We Now and Where Are We Heading?Viruses · 2024Review
- Upstream Stimulatory Factors Regulate HIV-1 Latency and Are Required for Robust T Cell Activation.Viruses · 2023Article
- TRIM24 controls induction of latent HIV-1 by stimulating transcriptional elongation.Communications biology · 2023Article
- An additional NF-κB site allows HIV-1 subtype C to evade restriction by nuclear PYHIN proteins.Cell reports · 2021Article
- The Evolution of Regulatory Elements in the Emerging Promoter-Variant Strains of HIV-1 Subtype C.Frontiers in microbiology · 2021Article
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- BK polyomavirus diversity-Why viral variation matters.Reviews in medical virology · 2020Review
- Cat and Mouse: HIV Transcription in Latency, Immune Evasion and Cure/Remission Strategies.Viruses · 2019Review
- Distinctive variation in the U3R region of the 5' Long Terminal Repeat from diverse HIV-1 strains.PloS one · 2018Article
- HIV-1 Promoter Single Nucleotide Polymorphisms Are Associated with Clinical Disease Severity.PloS one · 2016Article
- Functional properties of the HIV-1 long terminal repeat containing single-nucleotide polymorphisms in Sp site III and CCAAT/enhancer binding protein site I.Virology journal · 2014Article
- Genotypic and phenotypic heterogeneity in the U3R region of HIV type 1 subtype C.AIDS research and human retroviruses · 2014Article
- Genetic variation and HIV-associated neurologic disease.Advances in virus research · 2013Review
- Article
- Multiple NF-κB sites in HIV-1 subtype C long terminal repeat confer superior magnitude of transcription and thereby the enhanced viral predominance.The Journal of biological chemistry · 2012Article
- Sequence insertions in the HIV type 1 subtype C viral promoter predominantly generate an additional NF-κB binding site.AIDS research and human retroviruses · 2012Article
- CTGC motifs within the HIV core promoter specify Tat-responsive pre-initiation complexes.Retrovirology · 2012Article
- Nef functions in BLT mice to enhance HIV-1 replication and deplete CD4+CD8+ thymocytes.Retrovirology · 2012Article
- Identification and functional analysis of a second RBF-2 binding site within the HIV-1 promoter.Virology · 2011Article
- Structural and functional studies of CCAAT/enhancer binding sites within the human immunodeficiency virus type 1 subtype C LTR.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite extensive in vitro studies identifying a myriad of cellular transcription factors that bind the human immunodeficiency virus type 1 5' long terminal repeat (LTR), the relative contribution of these factors to human immunodeficiency virus type 1 replication in infected individuals remains obscure. To address this question, we investigated 478 proviral quasispecies derived from uncultured peripheral blood mononuclear cells of 42 patients representing all stages of infection. In addition to highly conserved TATA box, SP-1, and NF-kappaB sites, the Ets core and an adjacent 5'-ACYGCTGA-3' motif were extremely conserved. Importantly, the most frequent naturally occurring length polymorphism (MFNLP) duplicated 5'-ACYGCTGA-3' motifs in LTRs in which this same motif was disrupted or in LTRs in which a single point mutation to the Ets core ablated binding of c-Ets 1 and another factor distinct from both c-Ets 1 and Elf 1. The MFNLP's location was precise (position -121) and surprisingly frequent (38% of patients) and demarcated LTR Nef-coding sequences from LTR noncoding sequences that appear to be evolving independently. Aside from these features, we found no definitive clinical or transcription phenotype common to all MFNLP LTRs. We also found previously described and novel point polymorphisms, including some conferring TAR-dependent and TAR- independent Tat unresponsiveness, and showed that differential binding of nuclear factor(s) to a TCTAA TATA box variant may be the mechanism for the latter.
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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.