The lack of ADE that we observed with DENV-immune mouse sera contrasts with enhanced ZIKV pathogenesis described in Stat2−/− mice that were passively transferred DENV-immune human plasma;12 this disparity may be due to differences in the plasma-derived Ab preparations and/or mouse models (WT and Ifnar1−/− vs. Stat2−/−). The gene discussed is IFNAR1; the disease is acute disseminated encephalomyelitis.