ArticleProceedings of the National Academy of Sciences of the United States of America2002
Increased cell proliferation, but not reduced cell death, induces lymphocytosis in bovine leukemia virus-infected sheep.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 59 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
- Transcriptomics Profiling Identifies Cisplatin-Inducible Death Receptor 5 Antisense Long Non-coding RNA as a Modulator of Proliferation and Metastasis in HeLa Cells.Frontiers in cell and developmental biology · 2021Article
- Ablation of non-coding RNAs affects bovine leukemia virus B lymphocyte proliferation and abrogates oncogenesis.PLoS pathogens · 2020Article
- Memory CD4 T cell subsets are kinetically heterogeneous and replenished from naive T cells at high levels.eLife · 2017Article
- How Does HTLV-1 Undergo Oncogene-Dependent Replication Despite a Strong Immune Response?Frontiers in microbiology · 2017Article
- Recent Advances in BLV Research.Viruses · 2015Review
- Modes of Human T Cell Leukemia Virus Type 1 Transmission, Replication and Persistence.Viruses · 2015Review
- Interaction between Bovine leukemia virus (BLV) infection and age on telomerase misregulation.Veterinary research communications · 2015Article
- Review
- Quantifying T lymphocyte turnover.Journal of theoretical biology · 2013Article
- A mechanistic model for bromodeoxyuridine dilution naturally explains labelling data of self-renewing T cell populations.Journal of the Royal Society, Interface · 2013Article
- Animal models on HTLV-1 and related viruses: what did we learn?Frontiers in microbiology · 2012Article
- Reduced levels of reactive oxygen species correlate with inhibition of apoptosis, rise in thioredoxin expression and increased bovine leukemia virus proviral loads.Retrovirology · 2009Article
- Article
- Mechanisms of leukemogenesis induced by bovine leukemia virus: prospects for novel anti-retroviral therapies in human.Retrovirology · 2007Review
- Spleen-dependent turnover of CD11b peripheral blood B lymphocytes in bovine leukemia virus-infected sheep.Journal of virology · 2006Article
- Peripheral blood B-cell death compensates for excessive proliferation in lymphoid tissues and maintains homeostasis in bovine leukemia virus-infected sheep.Journal of virology · 2006Article
- Quantifying lymphocyte kinetics in vivo using carboxyfluorescein diacetate succinimidyl ester (CFSE).Proceedings. Biological sciences · 2006Article
- Naïve T-cell dynamics in human immunodeficiency virus type 1 infection: effects of highly active antiretroviral therapy provide insights into the mechanisms of naive T-cell depletion.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymphocyte homeostasis is the result of a critical balance between cell proliferation and death. Disruption of this subtle equilibrium can lead to the onset of leukemia, an increase in the number of lymphocytes being potentially due to both of these parameters. The relative importance of cell proliferation vs. apoptosis during pathogenesis induced by the primate T cell lymphotropic viruses and bovine leukemia virus (BLV) has been difficult to assess because of conflicting data from a range of in vitro and ex vivo experimental systems. Here, we aim to resolve this issue by measuring the rates of cell proliferation and death in the BLV-ovine system, an animal model of human T lymphotropic virus (HTLV-1). We use a method based on the i.v. injection of 5-bromodeoxyuridine into BLV-infected sheep. We show that B lymphocytes in BLV(+) asymptomatic sheep proliferate significantly faster than in uninfected controls (average proliferation rate: 0.020 per day vs. 0.011 per day). In contrast, the rates of cell death were not significantly different between aleukemic BLV-infected and control sheep (average death rate 0.089 per day vs. 0.094 per day, respectively). We conclude that the increase in the number of B cells during BLV-induced lymphocytosis results from higher proliferation rates but is not due to a significant decrease in apoptosis, in contrast to data from in vitro (ex vivo) experiments. The imbalance created by the net increase in proliferation in the absence of compensating cell death reveals a complex mechanism of feedback regulation controlling homeostasis in the blood compartment.
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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.