ArticleJournal of virology1997
Identification of a replication-competent pathogenic human immunodeficiency virus type 1 with a duplication in the TCF-1alpha region but lacking NF-kappaB binding sites.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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
15 citing papers in PubMed, 33 citations in OpenAlex.
- The Evolution of Regulatory Elements in the Emerging Promoter-Variant Strains of HIV-1 Subtype C.Frontiers in microbiology · 2021Article
- Cat and Mouse: HIV Transcription in Latency, Immune Evasion and Cure/Remission Strategies.Viruses · 2019Review
- Primate Lentiviruses Modulate NF-κB Activity by Multiple Mechanisms to Fine-Tune Viral and Cellular Gene Expression.Frontiers in microbiology · 2017Review
- Vitamin D3 inhibits TNFα-induced latent HIV reactivation in J-LAT cells.Molecular and cellular biochemistry · 2016Article
- 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
- In search of a function for the most frequent naturally-occurring length polymorphism (MFNLP) of the HIV-1 LTR: retaining functional coupling, of Nef and RBF-2, at RBEIII?International journal of biological sciences · 2007Review
- Genetic analysis of the long terminal repeat (LTR) promoter region in HIV-1-infected individuals with different rates of disease progression.Virus genes · 2007Article
- Antigenic stimulation specifically reactivates the replication of archived simian immunodeficiency virus genomes in chronically infected macaques.Journal of virology · 2005Article
- TFII-I regulates induction of chromosomally integrated human immunodeficiency virus type 1 long terminal repeat in cooperation with USF.Journal of virology · 2005Article
- Human immunodeficiency virus type 1 subtypes have a distinct long terminal repeat that determines the replication rate in a host-cell-specific manner.Journal of virology · 2004Article
- Naturally occurring human immunodeficiency virus type 1 long terminal repeats have a frequently observed duplication that binds RBF-2 and represses transcription.Journal of virology · 1998Article
- Divergent transcriptional regulation among expanding human immunodeficiency virus type 1 subtypes.Journal of virology · 1997Article
- CCAAT/enhancer binding protein (C/EBP) sites are required for HIV-1 replication in primary macrophages but not CD4(+) T cells.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- The kappaB sites in the human immunodeficiency virus type 1 long terminal repeat enhance virus replication yet are not absolutely required for viral growth.Journal of virology · 1997Article
- Genotypic and phenotypic characterization of long terminal repeat sequences from long-term survivors of human immunodeficiency virus type 1 infection.Journal of virology · 1997Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple human immunodeficiency virus type 1 (HIV-1) sequences with deletions of NF-kappaB binding sites at both the 5' and 3' long terminal repeats (LTRs) were identified in serial samples collected from an infected individual. The effect of this deletion on the level of transcription was studied by transient transfection of an LTR-driven luciferase reporter gene and by infection with a full-length recombinant HIV-1 containing a luciferase reporter (HIVHXBluc). Detectable levels of gene expression were found in both systems, in the presence or absence of the viral transactivator Tat. Interestingly, a duplication of a putative TCF-1alpha motif was found in place of the NF-kappaB elements in these viruses. Higher transcriptional activity was observed with HXBLTR (NF-kappaB intact) than with the patient's LTR (NF-kappaB deleted), suggesting that the NF-kappaB binding sites may promote optimal levels of viral gene transcription. The ability of these viruses with NF-kappaB deleted to replicate and cause substantial decline in CD4 cell counts demonstrates that the NF-kappaB binding sites are not absolutely required for viral replication or pathogenicity in vivo. These results are consistent with the notion that the HIV-1 LTR possesses functional redundancy which allows it to interact with multiple transcription factors, thereby ensuring viral replication in a variety of cell types.
Indexed as
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What 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.