These data indicate that miR-UL22A contributes to the blockade in TGFβ signaling observed during HCMV infection but, unlike in CD34+ HPCs where mutation of miR-UL22A completely restores TGFβ signaling, other viral factors contribute to the reduction in SMAD3 transcript and protein levels during lytic infection. Here, TGFB1 is linked to cytomegalovirus infection.