NAD Metabolism Drives CTCF-Cohesin Chromatin Regulation in EBV-Transformed B-Cells

In EBV-transformed B-cells, dependence on the NAD salvage pathway sustains PARP1 activity that maintains CTCF/cohesin chromatin folding and loop extrusion.

• Why it matters: EBV latency relies on stable viral chromatin organization, but PARP1’s high NAD use creates a metabolic burden that could limit architectural maintenance and latent gene expression.
• What they did: The study tested whether NAD salvage supports PARP1-driven architecture by inhibiting NAMPT with FK866 and by perturbing NAD levels, then assessing CTCF/cohesin chromatin remodeling and loop extrusion.
• The result: NAMPT inhibition phenocopied PARP1-linked chromatin disruption, altered CTCF/cohesin architectural remodeling, and reduced tumor burden in EBV xenograft models, revealing a therapeutic vulnerability.

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