CD59 protein functions as a negative regulator of the terminal pathway of the complement system by binding to the C8/C9 factors. To date, little is known about the role of CD59 in coronavirus infectious bronchitis virus (IBV) infection. In this study, we discovered that CD59 was downregulated in IBV-infected cells and was associated with IBV virions. This association protected IBV particles from antibody-dependent complement-mediated lysis. IBV titres in the supernatant were significantly increased when CD59 proteins were overexpressed in cells followed by IBV infection, and this observation was further supported by knockdown or cleavage of CD59. Because no considerable change in IBV N protein and viral RNA levels was detected in total cell lysates prepared from the overexpression, knockdown or cleavage of CD59 groups, our data indicated that CD59 was involved in IBV particle release and that IBV had evolved a mechanism to utilize CD59 to evade complement-mediated destruction.

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