ArticleJournal of virology1996
Cellular pathways involved in the ex vivo expression of bovine leukemia virus.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- The Complexity of Bovine Leukemia Virus Oncogenesis.Viruses · 2025Review
- Reduction of antisense transcription affects bovine leukemia virus replication and oncogenesis.PLoS pathogens · 2024Article
- Seroprevalence and detection of bovine leukosis virus in semen from breeding bulls in Costa Rica.Tropical animal health and production · 2023Article
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- Ablation of non-coding RNAs affects bovine leukemia virus B lymphocyte proliferation and abrogates oncogenesis.PLoS pathogens · 2020Article
- Detection of Bovine Leukemia Virus RNA in Blood Samples of Naturally Infected Dairy Cattle.Veterinary sciences · 2019Article
- How Does HTLV-1 Undergo Oncogene-Dependent Replication Despite a Strong Immune Response?Frontiers in microbiology · 2017Article
- Chemoresistance to Valproate Treatment of Bovine Leukemia Virus-Infected Sheep; Identification of Improved HDAC Inhibitors.Pathogens (Basel, Switzerland) · 2012Article
- Animal models on HTLV-1 and related viruses: what did we learn?Frontiers in microbiology · 2012Article
- Chromatin disruption in the promoter of bovine leukemia virus during transcriptional activation.Nucleic acids research · 2011Article
- Review
- 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
- Mechanisms of leukemogenesis induced by bovine leukemia virus: prospects for novel anti-retroviral therapies in human.Retrovirology · 2007Review
- A mutant form of the tax protein of bovine leukemia virus (BLV), with enhanced transactivation activity, increases expression and propagation of BLV in vitro but not in vivo.Journal of virology · 2003Article
- Inhibition of histone deacetylases induces bovine leukemia virus expression in vitro and in vivo.Journal of virology · 2002Article
- The region between amino acids 245 and 265 of the bovine leukemia virus (BLV) tax protein restricts transactivation not only via the BLV enhancer but also via other retrovirus enhancers.Journal of virology · 2000Article
- gammadelta(+) T-Lp6phocyte cytotoxicity against envelope-expressing target cells is unique to the alymphocytic state of bovine leukemia virus infection in the natural host.Journal of virology · 2000Article
- Antiviral activity of shiga toxin 1: suppression of bovine leukemia virus-related spontaneous lymphocyte proliferation.Infection and immunity · 2000Article
- Prostaglandin E(2) increases bovine leukemia virus tax and pol mRNA levels via cyclooxygenase 2: regulation by interleukin-2, interleukin-10, and bovine leukemia virus.Journal of virology · 2000Article
- Complete bovine leukemia virus (BLV) provirus is conserved in BLV-infected cattle throughout the course of B-cell lymphosarcoma development.Journal of virology · 1998Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bovine leukemia virus (BLV) is the etiologic agent of enzootic bovine leukosis. The virus adopts a strategy based on the lack of viral expression in vivo; only very rare BLV-infected B lymphocytes express viral information. When the cells are isolated from animals in persistent lymphocytosis and cultivated ex vivo, a tremendous increase in viral expression occurs. To gain insight into this mechanism, we employed a general approach using chemicals that interfere specifically with cellular pathways involved in signal transduction from the cell membrane to the nucleus. Our data demonstrate that BLV expression is not correlated with the activity of protein kinase A (PKA) and is even inhibited by cyclic AMP (cAMP). The cAMP/PKA pathway is thus apparently not involved in ex vivo viral expression. In contrast, PKC appears to play a key role in this process. Phorbol myristate acetate can directly activate viral expression in B cells (in the absence of T cells). Furthermore, calphostin C, a highly specific inhibitor of PKC, partly decreases ex vivo BLV expression. Our data further demonstrate that calmodulin and calcineurin, a calmodulin-dependent phosphatase, play a key role in the induction of viral expression. The involvement of this calmodulin-dependent pathway could explain the induction of expression that cannot be assigned to PKC. Furthermore, it appears that the activation of viral expression requires a calmodulin but not a PKA-dependent pathway. These data highlight major differences between transient transfection and ex vivo experiments. Finally, despite their homologies, BLV and human T-cell leukemia virus appear to use different signal transduction pathways to induce viral expression.
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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.