ArticleFrontiers in veterinary science2022
Enhanced pathogenicity by up-regulation of A20 after avian leukemia subgroup a virus infection.
Article in Frontiers in veterinary science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Residues Y142, I143, T146, Q206, S215, R228, G267, and M268 in the surface glycoprotein of FGV-like subgroup A avian leukosis virus are the key sites determining Tva receptor binding and infectivity.Veterinary research · 2026Article
- The Dual Role of A20 (TNFAIP3) in Viral Infection: A Context-Dependent Regulator of Immunity and Pathogenesis.Viruses · 2025Review
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Avian leukemia virus subgroup A (ALV-A) infection slows chicken growth, immunosuppression, and tumor occurrence, causing economic loss to the poultry industry. According to previous findings, A20 has a dual role in promoting and inhibiting tumor formation but has rarely been studied in avians. In this study, A20 overexpression and shRNA interference recombinant adenoviruses were constructed and inoculated into chicken embryos, and ALV-A (rHB2015012) was inoculated into 1-day-old chicks. Analysis of body weight, organ index, detoxification, antibody production, organ toxin load, and Pathological observation revealed that A20 overexpression could enhance ALV-A pathogenicity. This study lays the foundation for subsequent exploration of the A20-mediated tumorigenic mechanism of ALV-A.
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