These experiments revealed that infection with a “wild type” EBV modestly induced p16INK4a transcription in the first few days after infection – when EBNA2 transactivates inducers of cell cycle progression (e.g., MYC and cyclin D2) and a period of hyperproliferation has been described (Sinclair et al., 1994; Spender et al., 1999; Nikitin et al., 2010). Here, CCND2 is linked to infection.