Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion

Wenbiao Wang, Geng Li, Wu De, Zhen Luo, Pan Pan, Mingfu Tian, Yingchong Wang, Feng Xiao, Aixin Li, Kailang Wu, Xiaohong Liu, Lang Rao, Fang Liu (), Yingle Liu () and Jianguo Wu ()
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Wenbiao Wang: Wuhan University
Geng Li: Guangzhou University of Chinese Medicine
Wu De: Center for Disease Control and Prevention of Guangdong
Zhen Luo: Jinan University
Pan Pan: Wuhan University
Mingfu Tian: Wuhan University
Yingchong Wang: Wuhan University
Feng Xiao: Wuhan University
Aixin Li: Wuhan University
Kailang Wu: Wuhan University
Xiaohong Liu: Guangzhou University of Chinese Medicine
Lang Rao: Wuhan University
Fang Liu: Wuhan University
Yingle Liu: Wuhan University
Jianguo Wu: Wuhan University

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract Zika virus (ZIKV) infection is a public health emergency and host innate immunity is essential for the control of virus infection. The NLRP3 inflammasome plays a key role in host innate immune responses by activating caspase-1 to facilitate interleukin-1β (IL-1β) secretion. Here we report that ZIKV stimulates IL-1β secretion in infected patients, human PBMCs and macrophages, mice, and mice BMDCs. The knockdown of NLRP3 in cells and knockout of NLRP3 in mice inhibit ZIKV-mediated IL-1β secretion, indicating an essential role for NLRP3 in ZIKV-induced IL-1β activation. Moreover, ZIKV NS5 protein is required for NLRP3 activation and IL-1β secretion by binding with NLRP3 to facilitate the inflammasome complex assembly. Finally, ZIKV infection in mice activates IL-1β secretion, leading to inflammatory responses in the mice brain, spleen, liver, and kidney. Thus we reveal a mechanism by which ZIKV induces inflammatory responses by facilitating NLRP3 inflammasome complex assembly and IL-1β activation.

Date: 2018
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DOI: 10.1038/s41467-017-02645-3

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