To analyze the relevance of Dot1L in virus replication, we transduced A549 cells with lentiviruses expressing the Dot1L silencers or control shRNA (5 days), followed by infection with the PR8hv (Fig. 3C) or CAL07 (Fig. 3D) strains at low m.o.i. In agreement with the results observed with the Dot1L inhibitor, Dot1L downregulation produced an increase in viral replication. The gene discussed is DOT1L; the disease is infection.