ArticleVeterinary research communications2015
Interaction between Bovine leukemia virus (BLV) infection and age on telomerase misregulation.
Article in Veterinary research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 13 citations in OpenAlex.
- Infection-Induced Telomere Length Variation: Insights into Pathogenesis of Koala Retrovirus.Viruses · 2025Article
- Cell Immortality:Life (Basel, Switzerland) · 2024Review
- Review
- Post-Translational Protein Deimination Signatures in Serum and Serum-Extracellular Vesicles ofInternational journal of molecular sciences · 2020Article
- In silico and in vitro analysis of boAP3d1 protein interaction with bovine leukaemia virus gp51.PloS one · 2018Article
- Bovine leukaemia virus DNA in fresh milk and raw beef for human consumption.Epidemiology and infection · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bovine leukemia virus (BLV) is the causative agent of enzootic bovine leukosis (EBL). BLV can interact with telomerase and inhibits telomere shortening, contributing in leukemogenesis and tumour induction. The role of telomerase in BLV-induced lymphosarcoma and aging has been extensively studied. To date, the interaction of both BLV and aging on telomerase mis-regulation have, however, not been investigated. In the present study, telomerase activity in BLV positive and negative cows was compared over a wide range of ages (11-85 months). Lymphocyte counts were also measured in both BLV positive and negative groups. Telomerase activity was detected in all BLV infected animals with persistent lymphocytosis (PL), especially in older individuals. This study revealed that the cells undergo the natural telomerase shortening even in the presence of an existing viral infection. We also show that viral infection, especially during the PL phase of the disease, increases telomerase activity. A statistically significant interaction between age and viral infection was observed for telomere shortening during BLV infection. Older animals with BLV infection, especially those with persistent lymphocytosis or visible tumors, exhibited a sharp increase in telomerase activity. This study demonstrates that there is a significant interaction between BLV infection and telomerase up-regulation and lymphocytosis.
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