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Here, we sought to determine whether monocytes, which can cross tissue barriers, assist\u00a0ZIKV dissemination to the\u00a0fetus. We determined this by infecting monocytes with two strains of ZIKV: South American (PRVABC59) and Nigerian (IBH30656) and analyzing viral replication. We found that ZIKV infects and replicates in monocytes and\u00a0macrophages, which results in the modulation of a large number of cellular genes. Analysis of these genes identified multiple pathways including inflammasome to be targeted by ZIKV, which was confirmed by analyzing the transcript levels of the proteins of inflammasome pathways, NLRP3, ASC, caspase 1, IL-1 and IL-18. Interestingly, IFN\u03b1 and the IFN inducible gene, MxA were not enhanced, suggesting prevention of innate antiviral defense by ZIKV. Also, inhibition of inflammasome led to an increased transcriptional activity of IFN\u03b1, MxA and CXCL10. Based on these results we suggest that ZIKV transcription is regulated by inflammasomes.<\/jats:p>","DOI":"10.1038\/s41598-017-16072-3","type":"journal-article","created":{"date-parts":[[2017,11,16]],"date-time":"2017-11-16T12:26:32Z","timestamp":1510835192000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["ZIKV infection regulates inflammasomes pathway for replication in monocytes"],"prefix":"10.1038","volume":"7","author":[{"given":"S. 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