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Lymphomagenesis in the presence of deregulated  MYC  requires suppression of  MYC -driven apoptosis, often through downregulation of the pro-apoptotic  BCL2L11  gene (Bim). Transcription factors (EBNAs) encoded by the lymphoma-associated Epstein-Barr virus (EBV) activate  MYC  and silence  BCL2L11 . We show that the EBNA2 transactivator activates multiple  MYC  enhancers and reconfigures the  MYC  locus to increase upstream and decrease downstream enhancer-promoter interactions. EBNA2 recruits the BRG1 ATPase of the SWI/SNF remodeller to  MYC  enhancers and BRG1 is required for enhancer-promoter interactions in EBV-infected cells. At  BCL2L11 , we identify a haematopoietic enhancer hub that is inactivated by the EBV repressors EBNA3A and EBNA3C through recruitment of the H3K27 methyltransferase EZH2. Reversal of enhancer inactivation using an EZH2 inhibitor upregulates  BCL2L11  and induces apoptosis. EBV therefore drives lymphomagenesis by hijacking long-range enhancer hubs and specific cellular co-factors. EBV-driven  MYC  enhancer activation may contribute to the genesis and localisation of  MYC -Immunoglobulin translocation breakpoints in Burkitt's lymphoma.

MYC activation and BCL2L11 silencing by a tumour virus through the large-scale reconfiguration of enhancer-promoter hubs