FOXO3 and viral infectious disease: Indeed, we found that UL7, miR-US5-1, and miR-UL112-3p inactivation of FOXO3a is important to promote survival of CD34+ HPCs when they are independently expressed (Fig. 4C) as well as in the context of the viral infection, as demonstrated by the increased expression of BCL2L11 during infection with the HCMVΔmiR-US5-1+UL112-3p and ΔUL7 mutant viruses (Fig. 5D).