It may be possible that, at the early stages of infection, where the highest levels of T-Antigen are available, Survivin could potentially bind more efficiently to T-Antigen and co-localize to the nucleus (as observed in vitro and in vivo in oligodendrocytes from PML samples in the current study), with a potential effect on viral replication, whereas at later stages of infection, when T-Antigen transcription decreases and capsid proteins are produced, Survivin may be in excess, and therefore retain/recover its normal cytoplasmic localization and function as seen in bizarre astrocytes of PML. This evidence concerns the gene PML and infection.