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Differing Cytokine Expression Profiles in Chicken and Duck Mononuclear Cells in response to a Duck‐origin Avian Influenza Virus
Author(s) -
Adams Sean Cody,
Xing Zheng,
Cardona Carol Joy
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.561
Subject(s) - peripheral blood mononuclear cell , biology , immune system , virology , cytokine , influenza a virus subtype h5n1 , virus , immunology , interferon , ctl* , in vitro , biochemistry , cd8
Ducks are the reservoir hosts of avian influenza viruses (AIV) and do not display signs of disease when infected. AIV are frequently transmitted to chickens from free‐flying ducks where they may cause significant disease and pose a threat to the poultry industry because they can disrupt trade and reduce production. This difference in clinical disease may be due to the host's response to infection. In this report we focus on the expression of key cytokines and proteins: IL‐1 β, IL‐2, and the type I interferons and their expression in response to a duck‐origin AIV, in both host systems. Peripheral blood mononuclear cells (PBMC) from chickens and ducks, were cultured, and infected with AIV. The fold‐change in expression levels of antiviral cytokines was determined using RRTPCR. While both species responded to infection with a robust interferon response, IL‐1 β and IL‐2 cytokine responses differed dramatically. In ducks, IL‐1 β was strongly suppressed, while IL‐2 was induced nearly 30‐fold, implying the activation of a CTL response. In contrast, IL‐1 β was induced nearly 20‐fold in chicken PBMC over the course of the experiment, suggesting a strong pro‐inflammatory response, while IL‐2 expression remained at baseline levels. AIV infection of chicken PBMC induced significant cell death, whereas duck PBMC were viable at 36 hours pi. These cytokine responses indicate different strategies used by 2 species in response to AIV.