The Zika Virus (ZIKV) originally discovered in 1947 received little recognition as a serious infection until the WHO designated it as an international public health emergency in 2016. ZIKV is a flavivirus that has been linked to congenital ZIKV syndrome with symptoms including microcephaly. The Dengue Virus (DENV), another pathogenic flavivirus, has been associated with major infections including Dengue Hemorrhagic Fever and Dengue Shock Syndrome, but has not been linked to congenital symptoms. We hypothesize that this is due to ZIKV generating a stronger innate rather than adaptive immune response, whereas DENV is still initiating an innate immune response, but triggers a stronger adaptive immune response. By provoking the innate immune system, ZIKV is activating interferon (IFN) type 1 pathways, causing a cascade that ultimately activates Adenosine Deaminases acting on RNA (ADARs). If ADARs are dysregulated by ZIKV infection the changes in (mis)edited proteins may be responsible for observed neurodevelopmental defects. Using AIDD (a novel pipeline) and publically available RNA-seq datasets from three distinct human embryonic neural progenitor cell lines treated with either ZIKV or mock infection, we delineated gene expression patterns with a particular interest in ADAR1. Gene enrichment and pathway analysis was performed using DAVID and PANTHER. Our results indicate that ADAR1 is upregulated in two of the cell lines but not in the third, suggesting that the IFN type 1 pathway plays a significant role in ZIKV infection, and that changes in ADAR1 expression – and editing of neural targets - may be contributing to CZS symptoms.