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Using proximity labeling (TurboID-dCas9), ChIP-seq and DNA pull-down assays, we identified SMARCC2\u2014a BAF scaffolding subunit\u2014bound to cccDNA enhancer-promoter regions (Enh\u2160\/XP, CP\/EnhII), where it sustains nucleosome-depleted regions (NDRs) and recruits RNA polymerase II. Genetic or pharmacological BAF inhibition compacted cccDNA chromatin, reduced histone acetylation (AcH3\/AcH4), and enhanced SMC5\/6-mediated silencing to suppress transcription, with the BAF ATPase inhibitor FHT-2344 reducing serum HBV DNA by 50% (P &amp;lt;.05) and intrahepatic HBV RNA by 70% (P &amp;lt;.01) without cccDNA loss, indicating epigenetic silencing. Mechanistically, BAF maintains NDRs by counteracting nucleosome retention and recruiting host transcription factors such as HNF4\u03b1. This work concludes that BAF safeguards cccDNA chromatin plasticity to enable viral persistence, and targeting BAF (e.g. FHT-2344) epigenetically silences cccDNA, offering a novel strategy for functional cure.<\/jats:p>","DOI":"10.1093\/nar\/gkag073","type":"journal-article","created":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T12:44:12Z","timestamp":1769172252000},"source":"Crossref","is-referenced-by-count":3,"title":["Chromatin remodeler BAF maintains HBV cccDNA transcriptional competence and represents a therapeutic target"],"prefix":"10.1093","volume":"54","author":[{"given":"Dan","family":"Huang","sequence":"first","affiliation":[{"name":"Key Laboratory of Virology and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences , Wuhan 430071 ,","place":["China"]},{"name":"Medical School, University of Chinese Academy of Sciences , Beijing 100049 ,","place":["China"]},{"name":"Guangzhou National Laboratory, Guangzhou International Bio Island , Guangzhou 510005 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