Cell cycle progression of host cells can be modulated by viruses through influences on host cell cyclin-dependent kinases (CDKs). As an example, CDK9 has been implicated in infection by herpes simplex virus type 1 (HSV-1) (Table 1) (61). Specifically, CDK9 was shown for HSV-1 to be involved in expression of genes controlled by the viral regulatory protein, ICP22, and through binding to ICP22 leads to phosphorylation of RNA polymerase II (61). Palbociclib, at least partly through inhibition of CDK6, inhibited HSV-1 replication in vitro (62), likely through blockade of cellular protein phosphorylation (62). CDK9-targeting alvocidib showed activity against influenza A (Table 1) (63). CDK9 has been found to mediate the activity of RdRp of the influenza virus; cells lacking CDK9 showed impairment of viral replication (64).