AKT1 and infection: In agreement with our results showing a significant downregulation of Akt activity following infection by SpnWT, but not by mutant SpnΔlctOΔspxB, oxidation of regulatory cysteine residues by H2O2 was shown to inactivate Akt kinase and Fibroblast growth factor receptor (FGFR) kinase (39, 40).