To confirm this result in MDMs, we took advantage of three approaches: (i) knockdown of hUNG2 activity by transfection with a plasmid vector that overexpressed the potent uracil DNA glycosylase inhibitor protein (Ugi) (Bennett et al., 1993), (ii) overexpression of hUNG2 by transfection with a plasmid expression vector, and (iii) infections with viral constructs where virus protein R (Vpr) was deleted. Here, TCN1 is linked to infection.