Zika virus (ZIKV) is an emerging mosquito-borne flavivirus and is transmitted by daytime-active aedes mosquitoes. ZIKV was first identified in Zika forest, Uganda in 1947 and related to the dengue, yellow fever, Japanese encephalitis, and West Nile viruses. ZIKV infection often causes no or only mild symptoms, similar to a mild form of dengue fever. By far, ZIKV infection are not able to be prevented by medications or vaccines. In 2015, there was a significant increase in reports of ZIKV infection in the Americas. Brazil is the most affected country, with preliminary estimates of 440,000 to 1.3 million cases of autochthonous ZIKV infection reported through December 2015. Several recent reports from the Ministry of Health of Brazil indicates a possible association between ZIKV infection in pregnancy and fetal malformations. As of February 4, 2016, the ZIKV epidemic has continued to spread in many countries, and evidence of local ZIKV infection cases has been reported from 31 countries within the past 2 months, and 36 countries in the past 9 months. Although ZIKV infection has been linked to microcephaly among newborn infants recently, how ZIKV infection triggers cell death (especially apoptosis) in the brain is still largely unknown.
In this project I conducted a global transcriptome analysis of RNA sequencing data to identify and compare cellular genes and signaling pathways that are disregulated in the mouse brain following infection with ZIKV. These diregulated genes and signaling pathways might contribute to ZIKV pathogenesis within the CNS and serve as potential therapeutic targets for treatment of ZIKV associated brain abnormalities.