WenjunZhao, XuefengLi, HuixinLi, ZongxiHan, FangfangWang, ChenggangLiu, YuhaoShao, DeyingMa.
Comp Immunol Microbiol Infect Dis. 2019 Dec 18;68:101404. doi: 10.1016/j.cimid.2019.101404. [Epub ahead of print]
Fowl adenovirus (FAdV), as the causative agent of hepatitis-hydropericardium syndrome (HHS), poses a significant threat to the poultry industry in China in recent years. In this study, we investigated the immunopathogenesis of a FAdV-4 strain HN/151025 in 60-day-old chickens. The virus was highly virulent in chickens, with a broader tissue tropism in chickens, causing 60 % mortality. Postmortem findings of dead chickens showed mild HHS and liver degeneration and necrosis. Importantly, FAdV-4 infection induced significant upregulation of genes encoding most toll-like receptors, some cytokines (interleukin-1β, 2, 6, 8, and 18, and interferon-γ), most of avian β-defensins, myeloid differentiation primary response protein 88, p38 mitogen-activated protein kinases, and inducible nitric oxide synthase, in tissues of infected chicken, especially in spleen and bursa of Fabricius. There was also a significant positive correlation between FAdV-4 genome load and the mRNA expression levels of most of these factors in specific infected tissues. The results indicated the potential role of these proteins in host immune response against FAdV-4 infection. However, overexpression of these proteins might contribute to tissue damage of FAdV-4 infected chickens, and eventually lead to chicken death.
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Avian β-defensins; Chicken; Cytokines; Fowl adenovirus 4; Pathogenicity; Toll-like receptors