ArticleJournal of virology1998
An interferon regulatory factor binding site in the U5 region of the bovine leukemia virus long terminal repeat stimulates Tax-independent gene expression.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 35 citations in OpenAlex.
- Interferon dynamics in deltaretroviruses: why HTLV-1 evades, but BLV responds.Molecular biology reports · 2026Review
- The KT Jeang retrovirology prize 2025: Carine Van Lint.Retrovirology · 2026Article
- A complex network of transcription factors and epigenetic regulators involved in bovine leukemia virus transcriptional regulation.Retrovirology · 2023Review
- Role of the cellular factor CTCF in the regulation of bovine leukemia virus latency and three-dimensional chromatin organization.Nucleic acids research · 2022Article
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- Article
- Bovine leukemia virus long terminal repeat variability: identification of single nucleotide polymorphisms in regulatory sequences.Virology journal · 2018Article
- MicroRNAs Encoded by Bovine Leukemia Virus (BLV) Are Associated with Reduced Expression of B Cell Transcriptional Regulators in Dairy Cattle Naturally Infected with BLV.Frontiers in veterinary science · 2017Article
- Characterization of new RNA polymerase III and RNA polymerase II transcriptional promoters in the Bovine Leukemia Virus genome.Scientific reports · 2016Article
- Article
- A detailed molecular analysis of complete bovine leukemia virus genomes isolated from B-cell lymphosarcomas.Veterinary research · 2013Article
- Functional analysis of the interferon-stimulated response element of porcine circovirus type 2 and its role during viral replication in vitro and in vivo.Virology journal · 2012Article
- Chromatin disruption in the promoter of bovine leukemia virus during transcriptional activation.Nucleic acids research · 2011Article
- DNA cytosine methylation in the bovine leukemia virus promoter is associated with latency in a lymphoma-derived B-cell line: potential involvement of direct inhibition of cAMP-responsive element (CRE)-binding protein/CRE modulator/activation transcription factor binding.The Journal of biological chemistry · 2010Article
- Effect of type-I interferon on retroviruses.Viruses · 2009Article
- Mechanisms of leukemogenesis induced by bovine leukemia virus: prospects for novel anti-retroviral therapies in human.Retrovirology · 2007Review
- Article
- Inhibition of histone deacetylases induces bovine leukemia virus expression in vitro and in vivo.Journal of virology · 2002Article
- Suboptimal enhancer sequences are required for efficient bovine leukemia virus propagation in vivo: implications for viral latency.Journal of virology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bovine leukemia virus (BLV) replication is controlled by both cis- and trans-acting elements. The virus-encoded transactivator, Tax, is necessary for efficient transcription from the BLV promoter, although it is not present during the early stages of infection. Therefore, sequences that control Tax-independent transcription must play an important role in the initiation of viral gene expression. This study demonstrates that the R-U5 sequence of BLV stimulates Tax-independent reporter gene expression directed by the BLV promoter. R-U5 was also stimulatory when inserted immediately downstream from the transcription initiation site of a heterologous promoter. Progressive deletion analysis of this region revealed that a 46-bp element corresponding to the 5' half of U5 is principally responsible for the stimulation. This element exhibited enhancer activity when inserted upstream or downstream from the herpes simplex virus thymidine kinase promoter. This enhancer contains a binding site for the interferon regulatory factors IRF-1 and IRF-2. A 3-bp mutation that destroys the IRF recognition site caused a twofold decrease in Tax-independent BLV long terminal repeat-driven gene expression. These observations suggest that the IRF binding site in the U5 region of BLV plays a role in the initiation of virus replication.
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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 Socratic graph.