CDK2 and infection: Moreover, as the non-cycling PXB cells likely had little to no CDK2 activity, the inhibition of CCC DNA formation during HBV infection of these cells further suggests that the endogenous CDK2 packaged into the HBV capsids was targeted by the inhibitors during infection to block NC phosphorylation, uncoating, and CCC DNA formation, thus implicating the endogenous CDK2 in these critical processes.