PRKAA2 and infection: Treatment with this drug inhibited RVFV less than 2 fold in AMPKα1/AMPKα2−/− MEFs and was not significant, whereas infection was inhibited greater than 5-fold in the wild type cells (Figure S4A) with no toxicity in either cell type (Figure S4B), indicating that the major action of this drug was through AMPK as previously published [46], [47].