ArticleViruses2022
Synergistic Immunosuppression of Avian Leukosis Virus Subgroup J and Infectious Bursal Disease Virus Is Responsible for Enhanced Pathogenicity.
Article in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Illuminating the pathological, immunohistochemical, and molecular investigations of myelocytomatosis in chicken embryos.Infectious agents and cancer · 2026Article
- Revealing novel and conservative CD8Veterinary research · 2024Article
- A Comprehensive Analysis of the ceRNA Network and Hub Genes in Avian Leukosis Virus Subgroup J and Infectious Bursal Disease Virus Superinfection.Animals : an open access journal from MDPI · 2024Article
- Deciphering Immune Modulation in Chickens Co-Infected with ALV-J and CIAV: A Transcriptomic Approach.Microorganisms · 2024Article
- Immunopathological investigation and genetic evolution of Avian leukosis virus Subgroup-J associated with myelocytomatosis in broiler flocks in Egypt.Virology journal · 2024Article
- Synergy of Subgroup J Avian Leukosis Virus and Chicken Infectious Anemia Virus Enhances the Pathogenicity in Chickens.Microorganisms · 2024Article
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Authors and funding
8 authors.
Funding
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Abstract
In recent years, superinfections of avian leukosis virus subgroup J (ALV-J) and infectious bursal disease virus (IBDV) have been frequently observed in nature, which has led to the increasing virulence in infected chickens. However, the reason for the enhanced pathogenicity has remained unclear. In this study, we demonstrated an effective candidate model for studying the outcome of superinfections with ALV-J and IBDV in cells and specific-pathogen-free (SPF) chicks. Through in vitro experiments, we found that ALV-J and IBDV can establish the superinfection models and synergistically promote the expression of IL-6, IL-10, IFN-α, and IFN-γ in DF-1 and CEF cells. In vivo, the weight loss, survival rate, and histopathological observations showed that more severe pathogenicity was present in the superinfected chickens. In addition, we found that superinfections of ALV-J and IBDV synergistically increased the viral replication of the two viruses and inflammatory mediator secretions in vitro and in vivo. Moreover, by measuring the immune organ indexes and blood proportions of CD3
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