Stimulates viral immediate-early (IE) transcription. Plays a role in the inhibition of the host innate repsonse by targeting STING1 and thus the cGAS-STING pathway. Counteracts also host DAXX-mediated repression of viral transcription. Displaces a DAXX-binding protein, ATRX, from nuclear domain 10 sites (ND10) shortly after infection. Increases the basal level of SUMOylated DAXX in infected cells. Stimulates quiescent cells to re-enter the cell cycle, proceed through G1 and enter the S phase. Interacts with hypophosphorylated forms of RB1 and induces their degradation by the proteasome without involving ubiquitin conjugation. Interacts with the host protein DAXX; this interaction takes place at ND10 and induces the reversal of DAXX-mediated repression of viral transcription. Interacts with UL35. Interacts with host TMEM173/STING1; this interaction inhibits the cGAS/STING pathway. Interacts with host RB1; this interaction mediates RB1 proteasomal degradation. Present in the nucleus shortly after infection as well as during the late phase of viral morphogenesis. Detected at nuclear domain 10 (ND10). S-nitrosylation limits ability to undermine the cGAS/STING antiviral pathway. Belongs to the herpesviridae pp71 family.