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Reciprocal Regulation between Enterovirus 71 and the NLRP3 Inflammasome.

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journal contribution
posted on 17.02.2016, 00:00 authored by H. Wang, X. Lei, X. Xiao, C. Yang, W. Lu, Z. Huang, Q. Leng, Q Jin, B. He, G. Meng, J. Wang
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.


. This work was supported by grants from the National Key Basic Research Programs (2011CB504903, 2014CB541905, and 2015CB554302), the National Natural Science Foundation of China (81225014, 31370892, 31300712, 31270200, 31170868, and 91429307), National Major Projects for Science and Technology (2012ZX10002007-003 and 2014ZX0801011B-001), the Program for Changjiang Scholars and Innovative Research Team in Universities (IRT13007), the SA-SIBS Scholarship Program, and the CAS/SAFEA International Partnership Program for Creative Research Teams.


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This is the copy of an article published in Cell Reports © 2015 Elsevier Publications.





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