Zika virus, a single-stranded positive-sense RNA virus belonging to the Flaviviridae family, has been linked to a distinct pattern of birth defects and disabilities, as well as Guillain-Barre syndrome in healthy individuals. Proimmune™, free-form amino acids (FFAAP) reduce ZIKV replication by up to 90% in comparison to the mocked-infected cells. The mechanism by which ZIKV replication is reduced is puzzling because blocking intracellular glutathione biosynthesis is still associated with reduced ZIKV replication. Here we provide data generated to test the hypothesis Proimmune™ was sufficient to neutralize ROS, preventing the cell from inducing Oxeiptosis via nrf2 release from KEAP1 the usual innate defense engaged in the presence of pathogen-induced ROS. The data reveal that despite ROS generated post high multiplicity ZIKV infection, Proimmune™ reduces virus replication in the presence of glutathione biosynthesis inhibitors (BSO) and in the absence of ROS upregulation of nrf2-regulated genes that protect cells from excess oxygen free-radicals.