Abstract
Abstract Infectious Bursal Disease (IBD) is an acute, highly contagious and immunosuppressive avian disease caused by IBD virus (IBDV). Although IBDV-induced immuno-suppression has been well-established, the exact molecular mechanism for such induction is unclear. We report here that IBDV VP4 is an interferon-suppressor by interacting with the Glucocorticoid-induced leucine zipper (GILZ) in host cells. We found that VP4 suppressed the expression of type I interferon in HEK293T cells with Tumor Necrosis Factor(TNF)-α treatment or Sendai virus (SeV) infection, and this suppression could be completely abolished by knockdown of GILZ by siRNA. Furthermore, knockdown of GILZ significantly inhibited IBDV growth in host cells. Thus, VP4-induced suppression of type I interferon is mediated by interacting with GILZ, a protein that appears to inhibit cell responses to IBDV infection.
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