Regulation of the Epstein-Barr Epigenome by Histone Variant MacroH2A

MacroH2A is enriched at repetitive EBV elements and, when depleted or knocked out in EBV+ SNU719 and Mutu I cells, increases EBV DNA copy number and episome replication.

• Why it matters: EBV latency depends on stable episome maintenance, yet how histone variants shape EBV chromatin structure, gene programs, and genome integrity remains unclear.
• What they did: ChIP-seq mapped macroH2A enrichment at oriLyt, BHLF1, LF3, and TR regions; macroH2A depletion or CRISPR/Cas9 knockout was tested in EBV-associated gastric cancer and Burkitt lymphoma cells with RNA-seq and replication readouts.
• The result: MacroH2A loss increased H2A.Z and EBNA1 at oriP, linked gammaH2AX localization to macroH2A, reduced lytic gene activation during reactivation, and enhanced replication/episome maintenance of oriP-containing plasmids.

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