We hypothesize that this stability reflects not only viral oncogeneanchored enhancer scaffolds (e.g., EBNA2RBPJ and EBNA-LPmediated 3D looping), but also contributions from host chromatin remodelers (e.g., BRD4, CHD4/NuRD), DNA methylation writers and erasers (DNMTs, TET enzymes), and hypoxia-responsive transcription factors (HIF-1, HIF-2) that may cooperate with EBV oncoproteins such as EBNA2
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doi: 10.5173/ceju.2020.1975 135 WuXLuMYunDGaoSChenSHuLet al