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. 2019 Aug 14;10:1925. doi: 10.3389/fimmu.2019.01925

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Copyright © 2019 Liu, Tang, Tang, Pu, Gong, Fang, Zhang, Li, Zhu, Wang, Wu, Liao, Li, Zhou and Huang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic of the mechanism of AKI induced by ZIKV infection. ZIKV infection promotes NLRP3 inflammasome activation and IL-1β production in the kidney by suppressing the expression of Bcl-2. IL-1β attenuates the expression of aquaporins, thus leading to water re-absorption disorder and renal cell injury. In addition, ZIKV infection increases PARP and caspase-3-mediated renal apoptosis via inhibiting Bcl-2, which further enhances the kidney injury. Overall, ZIKV infection induces acute kidney injury through activating NLRP3 inflammasome via suppressing Bcl-2.