Open AccessClassical swine fever virus and p7 protein induce secretion of IL-1β in macrophages
Author(s) -
Lin Zhi,
Wan Liang,
Kai Kang,
Helin Li,
Zhi Cao,
Yanming Zhang
Publication year - 2014
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/vir.0.068502-0
Subject(s) - biology , secretion , innate immune system , classical swine fever , virus , virology , immune system , proteasome , downregulation and upregulation , immunology , microbiology and biotechnology , biochemistry , gene
Classical swine fever virus (CSFV) has a tropism for vascular endothelial cells and immune system cells. The process and release of pro-inflammatory 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 may not be involved in CSFV-mediated IL-1β release. Recently, research has indicated a novel mechanism by which inflammasomes are triggered through detection of activity of viroporin. We further demonstrated that CSFV viroporin p7 protein induced IL-1β secretion which could be inhibited by the ion channel blocker amantadine and also discovered that p7 protein was a short-lived protein degraded by the proteasome. Together, our observations provided an insight into the mechanism of CSFV-induced inflammatory responses.