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Although the DNA damage response (DDR) facilitates cccDNA biogenesis, its role in regulating cccDNA stability remains unclear. By intersecting published cccDNA-associated proteomic datasets with known DDR-related host factors, we identified heterogeneous nuclear ribonucleoprotein A2\/B1 (hnRNPA2B1) as a novel restriction factor that binds cccDNA and suppresses HBV replication by promoting cccDNA degradation. Mechanistically, hnRNPA2B1 interacted with the G-quadruplex (G4) structure of cccDNA, with preference for G4-1, G4-7, and G4-10, and leads to the recruitment of the cytidine deaminase APOBEC3B by its prion-like domain (PrLD), thereby inducing C&amp;gt;T and G&amp;gt;A hypermutations and initiating cccDNA decay. Notably, HBV counteracts this defense mechanism through HBx-mediated hnRNPA2B1 polyubiquitination and proteasomal degradation, revealing a viral evasion strategy that perpetuates cccDNA persistence. These findings reveal a G4-dependent surveillance axis wherein hnRNPA2B1 directs APOBEC3B-mediated cytidine deamination to destabilize cccDNA while identifying HBx-induced hnRNPA2B1 ubiquitination as a viral countermeasure. This mechanistic duality not only elucidates a critical virus-host interaction governing cccDNA persistence but also provides a promising therapeutic target for the treatment of HBV infection.<\/jats:p>","DOI":"10.1093\/nar\/gkag149","type":"journal-article","created":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T12:43:10Z","timestamp":1770813790000},"source":"Crossref","is-referenced-by-count":3,"title":["hnRNPA2B1 induces HBV cccDNA degradation by recruiting APOBEC3B"],"prefix":"10.1093","volume":"54","author":[{"given":"Zhendong","family":"Fu","sequence":"first","affiliation":[{"name":"Key Laboratory for Experimental Teratology of Ministry of Education, Key Laboratory of Infection and Immunity of Shandong Province and Dept. Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo Medical College, Shandong University , Jinan 250012 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liyuan","family":"Wang","sequence":"additional","affiliation":[{"name":"Key Laboratory of Immune Microenvironment and Inflammatory Disease Research in Universities of Shandong Province, School of Basic Medical Sciences, Shandong Second Medical University , Weifang 261053 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Sun","sequence":"additional","affiliation":[{"name":"Key Laboratory for Experimental Teratology of Ministry of Education, Key Laboratory of Infection and Immunity of Shandong Province and Dept. 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Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo Medical College, Shandong University , Jinan 250012 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaohong","family":"Liang","sequence":"additional","affiliation":[{"name":"Key Laboratory for Experimental Teratology of Ministry of Education, Key Laboratory of Infection and Immunity of Shandong Province and Dept. Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo Medical College, Shandong University , Jinan 250012 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8121-4718","authenticated-orcid":false,"given":"Chunhong","family":"Ma","sequence":"additional","affiliation":[{"name":"Key Laboratory for Experimental Teratology of Ministry of Education, Key Laboratory of Infection and Immunity of Shandong Province and Dept. 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