On the left (green), HCMV miR-US5–2 downregulates NAB1, thereby
alleviating the NAB1-induced inhibition of TGF-β expression. This leads
to an increase in TGF-β secretion and the subsequent myelosuppression of
neighboring uninfected cells. On the right (red), HCMV miR-UL22A-3p and
−5p downregulate SMAD3 and, as a result, make infected cells unresponsive
to TGF-β, which supports the maintenance of latency.