Zika Virus Impairs Host NLRP3-mediated Inflammasome Activation in an NS3-dependent Manner

Immune Network
Eunji GimJe-Wook Yu


Zika virus (ZIKV) is a mosquito-borne flavivirus associated with severe neurological disorders including Guillain-Barré syndrome and microcephaly. The host innate immune responses against ZIKV infection are essential for protection; however, ZIKV has evolved strategies to evade and antagonize antiviral responses via its nonstructural (NS) proteins. Here, we demonstrated that ZIKV infection unexpectedly inhibits NLRP3-dependent inflammasome activation in bone marrow-derived macrophages and mixed glial cells from mouse brain. ZIKV infection led to increased transcript levels of proinflammatory cytokines such as IL-1β and IL-6 via activating NF-κB signaling. However, ZIKV infection failed to trigger the secretion of active caspase-1 and IL-1β from macrophages and glial cells even in the presence of LPS priming or ATP costimulation. Intriguingly, ZIKV infection significantly attenuated NLRP3-dependent, but not absent in melanoma 2-dependent caspase-1 activation and IL-1β secretion from both cells. ZIKV infection further blocked apoptosis-associated speck-like protein containing a caspase recruitment domain oligomerization in LPS/ATP-stimulated macrophages. Interestingly, expression of ZIKV NS3 protein reduced NLRP3-mediated caspase...Continue Reading


Jul 23, 2005·Cell Death and Differentiation·J-W YuEmad S Alnemri
Jan 23, 2009·Nature·Teresa Fernandes-AlnemriEmad S Alnemri
Mar 23, 2010·Cell·Kate Schroder, Jürg Tschopp
Mar 31, 2010·Nature Immunology·Teresa Fernandes-AlnemriEmad S Alnemri
May 25, 2013·Nature Reviews. Immunology·Eicke LatzAndrea Stutz
Apr 29, 2014·Molecular Cell·Jason W Upton, Francis Ka-Ming Chan
Apr 19, 2016·Emerging Infectious Diseases·Robert S LanciottiLeticia Del Carmen Castillo Signor
May 24, 2016·Cell Host & Microbe·Alesha GrantAdolfo García-Sastre
Jun 2, 2016·Cell Host & Microbe·Kendra M QuickeMehul S Suthar
Jun 12, 2016·Current Opinion in Microbiology·Dia C Beachboard, Stacy M Horner
Jun 30, 2016·Lancet·Vivian I Avelino-Silva, Jeffrey N Martin
Oct 6, 2016·Cell·Theodore C Pierson, Barney S Graham
Oct 21, 2016·Scientific Reports·Hicham El CostaNabila Jabrane-Ferrat
Nov 1, 2016·EMBO Reports·Anil KumarTom C Hobman
Feb 6, 2017·Biochemical and Biophysical Research Communications·Paola Maura TricaricoPierlanfranco D'Agaro
May 5, 2017·Journal of Virology·Vidyanath ChaudharyDong-Yan Jin
May 20, 2017·Cell Death and Differentiation·Patrick F Connolly, Howard O Fearnhead
Nov 3, 2017·Immune Network·Keeton K KrauseMukesh Kumar
Jan 31, 2018·Nature Communications·Hongjie XiaPei-Yong Shi
Mar 9, 2018·The Journal of Infectious Diseases·Zhenjian HeMengfeng Li
Mar 15, 2018·The New England Journal of Medicine·Bruno HoenArnaud Fontanet
Jun 6, 2018·Frontiers in Immunology·Do-Wan Shim, Kwang-Ho Lee
Jun 20, 2018·Proceedings of the National Academy of Sciences of the United States of America·Qiang DingAlexander Ploss
Aug 31, 2018·Nature·Theodore C Pierson, Michael S Diamond
Sep 21, 2018·International Journal of Molecular Sciences·Ekaterina NikitinaJulia Kzhyshkowska
Jul 31, 2019·Nucleic Acids Research·Shan XuLei Shi


Feb 29, 2020·Pathogens·Aarón Oyarzún-ArrauRicardo Soto-Rifo

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