ArticleDevelopmental and comparative immunology2017
Early pathogenesis during infectious bursal disease in susceptible chickens is associated with changes in B cell genomic methylation and loss of genome integrity.
Article in Developmental and comparative immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 10 citations in OpenAlex.
- Infectious bursal disease virus suppresses humoral immunity via blocking antibody affinity maturation in chickens.iScience · 2026Article
- Infectious bursal disease virus replication is inhibited by avain T cell chemoattractant chemokine CCL19.Frontiers in microbiology · 2022Article
- Impacts of Epigenetic Processes on the Health and Productivity of Livestock.Frontiers in genetics · 2020Review
- Immunomodulatory Potential ofVaccines · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
We propose a model by which an increase in the genomic modification, 5-hydroxymethylcytosine (5hmC), contributes to B cell death within the chicken bursa of Fabricus (BF) infected with infectious bursal disease virus (IBDV). Our findings indicate that, following an IBDV infection, Rhode Island Red (RIR) chickens have fewer surviving B cells and higher levels of 5hmC in the BF than the more resistant 15l line of birds. Elevated genomic 5hmC levels within the RIR BF are associated with markers of immune responses: infiltrating T cells and increased expression of CD40L, FasL and iNOS. Such changes correlate with genomic fragmentation and the presence of IBDV capsid protein, VP2. To explore the effects of CD40L, the immature B cell line, DT40, was exposed to recombinant chicken CD40L that resulted in changes in nuclear 5hmC distribution. Collectively, our observations suggest that T cell infiltration exacerbates early immunopathology within the BF during an IBDV infection contributing to B cell genomic instability and death to facilitate viral egress and immunosuppression.
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Registered trials
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