Infection of both WNV and ZIKV in IL-22-/- mice led to alleviated clinical manifestations (Fig. 2) with decreased viral load and elevated pro-inflammatory TNF-α expression in the brain (Fig. 5a and S3) [15], whereas rIL-22 cytokine treatment in vivo played a detrimental role in ZIKV infection (Fig. 2e). The gene discussed is IL22; the disease is infection.