Classical swine fever virus (CSFV) has a tropism for vascular endothelial cells and immune system cells. The process and release of proinflammatory cytokines, including IL-1β and IL-18, is one of the fundamental reactions of the innate immune response to viral infection. In this study, we investigated the production of IL-1β from macrophages following CSFV infection. Our results showed that IL-1β was upregulated after CSFV infection through activating caspase-1. Subsequent studies demonstrated that reactive oxygen species (ROS) may not be involved in CSFV mediated IL-1β release. Recently, researchers indicate a novel mechanism by which inflammasomes are triggered through detection of activit... More
Classical swine fever virus (CSFV) has a tropism for vascular endothelial cells and immune system cells. The process and release of proinflammatory cytokines, including IL-1β and IL-18, is one of the fundamental reactions of the innate immune response to viral infection. In this study, we investigated the production of IL-1β from macrophages following CSFV infection. Our results showed that IL-1β was upregulated after CSFV infection through activating caspase-1. Subsequent studies demonstrated that reactive oxygen species (ROS) may not be involved in CSFV mediated IL-1β release. Recently, researchers indicate a novel mechanism by which inflammasomes are triggered through detection of activity of viroporin. We further demonstrated that CSFV viroporin p7 protein induces IL-1β secretion and also discovered that p7 protein is a short-lived protein degraded by the proteasome. Together, our observations provide an insight into the mechanism of CSFV-induced inflammatory response.
