BZLF1 expressed in the absence of EBV infection is also sufficient to induce phosphorylation and SUMOylation of TRIM33, which may be a result of the disruption of TRIM24/TRIM28/TRIM33 complexes and/or a conformational change in TRIM33 induced by interaction with BZLF1, making the TRIM33 sites accessible to endogenous kinases and SUMOylation machinery. This evidence concerns the gene TRIM33 and Epstein-Barr virus infection.