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
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