Dysregulated transcription in core- and pol-specific CD8 T cells can be targeted by HDAC inhibition to improve T-cell function in chronic hepatitis B.

Entinostat increases histone acetylation and improves CD8 T-cell function in core- and polymerase-specific cells from untreated, highly viremic, HBeAg-negative chronic hepatitis B patients.

• Why it matters: HBV persistence in chronic hepatitis B is linked to virus-specific CD8 T-cell dysfunction, but the transcriptional and epigenetic correlates of functional cure are not well defined.
• What they did: Core- and polymerase-specific CD8 T cells from untreated CHB patients were profiled by RNA sequencing and compared with cells from rNUC and rACU patients; histone acetylation, cytokines, and cytotoxic activity were then tested after histone deacetylase inhibition.
• The result: A shared 101-gene “resolution signature” distinguished resolution groups from CHB, and entinostat significantly increased histone acetylation levels and improved T-cell function, supporting HDAC inhibition as a therapeutic strategy.

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