IFI16 and infection: Thus, in line with the results of Cristea et al. [23] and Rolle et al. [24], our findings indicate that Herpesvirus replication, and in particular that of HCMV, may be impaired by IFI16 silencing in the first hours after infection at the lower MOI, but as virus replication progresses this impairment becomes lost as shown by increased viral yields compared to controls at the later time points p.i. At higher MOI, however, the relevance of IFI16 in the control of HCMV replication appears to be less.