Reciprocal Regulation between Enterovirus 71 and the NLRP3 Inflammasome. H. Wang X. Lei X. Xiao C. Yang W. Lu Z. Huang Q. Leng Q Jin B. He G. Meng J. Wang 10027/20271 https://indigo.uic.edu/articles/journal_contribution/Reciprocal_Regulation_between_Enterovirus_71_and_the_NLRP3_Inflammasome_/10780505 Enterovirus 71 (EV71) is the major etiological agent of hand, foot, and mouth disease (HFMD). Early studies showed that EV71-infected patients with severe complications exhibited elevated plasma levels of IL-1β, indicating that EV71 may activate inflammasomes. Our current study demonstrates that the NLRP3 inflammasome plays a protective role against EV71 infection of mice in vivo. EV71 replication in myeloid cells results in the activation of the NLRP3 inflammasome and secretion of IL-1β. Conversely, EV71 counteracts inflammasome activation through cleavage of NLRP3 by viral proteases 2A and 3C, which cleave NLRP3 protein at the G493-L494 or Q225-G226 junction, respectively. Moreover, EV71 3C interacts with NLRP3 and inhibits IL-1β secretion when expressed in mammalian cells. These results thus reveal a set of reciprocal regulations between enterovirus 71 and the NLRP3 inflammasome. 2016-02-17 00:00:00 untagged