Abstract:
:The covalently closed circular DNA (cccDNA) of hepatitis B virus (HBV) is a viral center molecule for HBV infection and persistence. However, the cellular restriction factors of HBV cccDNA are not well understood. Here, we show that TGF-β can induce nuclear viral cccDNA degradation and hypermutation via activation-induced cytidine deaminase (AID) deamination activity in hepatocytes. This suppression by TGF-β is abrogated when AID or the activity of uracil-DNA glycosylase (UNG) is absent, which indicates that AID deamination and the UNG-mediated excision of uracil act in concert to degrade viral cccDNA. Moreover, the HBV core protein promotes the interaction between AID and viral cccDNA. Overall, our results indicate a novel molecular mechanism that allows cytokine TGF-β to restrict viral nuclear cccDNA in innate immunity, thereby suggesting a novel method for potentially eliminating cccDNA.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Qiao Y,Han X,Guan G,Wu N,Sun J,Pak V,Liang Gdoi
10.1002/1873-3468.12058subject
Has Abstractpub_date
2016-02-01 00:00:00pages
419-27issue
3eissn
0014-5793issn
1873-3468journal_volume
590pub_type
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