After entering the cell, the viral genes are transcribed by host cell RNA polymerase II to produce early mRNAs. Because of the relative simplicity of the genome, polyomaviruses are heavily dependent on the cell for transcription and genome replication. The cis-acting regulatory element surrounding the origin of replication directs transcription, and T-antigen directs transcription and replication.<unk>  DNA replication is initiated by binding of<unk>  T-antigen to the origin region of the genome. The function of T-antigen is controlled by phosphorylation, which attenuates the binding to the<unk>  origin. Protein-protein interactions between T-antigen and DNA polymerase-alpha directly stimulate replication of the virus genome. T-antigen also binds and inactivates tumor suppressor proteins (p53, p105-Rb). This causes the cells to leave G1 phase and enter into S phase, which promotes DNA replication. The<unk>  genome is very small and does not encode all the information necessary for DNA replication. Therefore, it is essential for the host cell to enter S phase, when cell DNA and the viral genome are replicated together. Therefore, in addition to increasing transcription, another function of T-antigen is to alter the cellular environment to permit virus genome replication.
SV40 large T antigen
Adenovirus E1B protein
CccDNA
Long interspersed nuclear element
OTL-103
T independent antigen 
CAd3-ZEBOV
Kaposi's sarcoma-associated herpesvirus