Porcine reproductive and respiratory syndrome virus infection promotes C1QBP secretion to enhance inflammatory responses.

Complement component 1, q subcomponent binding protein (C1QBP) is a receptor for the globular heads of C1q and modulates various biological processes including infection, inflammation, autoimmunity, and cancer. In our previous study to identify differentially expressed secretory proteins in Marc-145 cells infected with porcine reproductive and respiratory syndrome virus (PRRSV), mass spectrum data showed that C1QBP was secreted after PRRSV infection. However, the biological significance of secreted C1QBP remains unclear. In this study, we confirmed that PRRSV infection promoted C1QBP secretion in Marc-145 cells and porcine alveolar macrophages (PAMs), the target cells of PRRSV in vivo. Knockdown of endogenous C1QBP decreased PRRSV-induced inflammatory responses. The purified recombinant porcine C1QBP (poC1QBP) had proinflammatory effects. The exogenous addition of poC1QBP significantly enhanced PRRSV-induced inflammatory responses and abolished the inhibitory effects mediated by poC1QBP-knockdown. Taken together, these results demonstrate that PRRSV infection promotes poC1QBP secretion that enhances inflammatory responses.
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