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FEBS Lett. 2013 Sep 17;587(18):3148-52. doi: 10.1016/j.febslet.2013.07.055. Epub 2013 Aug 15.

Concerted action of activation-induced cytidine deaminase and uracil-DNA glycosylase reduces covalently closed circular DNA of duck hepatitis B virus.

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1
Department of Molecular Genetics, Kanazawa University, Graduate School of Medical Sciences, Kanazawa, Japan.

Abstract

Covalently closed circular DNA (cccDNA) forms a template for the replication of hepatitis B virus (HBV) and duck HBV (DHBV). Recent studies suggest that activation-induced cytidine deaminase (AID) functions in innate immunity, although its molecular mechanism of action remains unclear, particularly regarding HBV restriction. Here we demonstrated that overexpression of chicken AID caused hypermutation and reduction of DHBV cccDNA levels. Inhibition of uracil-DNA glycosylase (UNG) by UNG inhibitor protein (UGI) abolished AID-induced cccDNA reduction, suggesting that the AID/UNG pathway triggers the degradation of cccDNA via cytosine deamination and uracil excision.

KEYWORDS:

3D-PCR; AID; APOBEC; Base excision repair; DHBV; Hepatitis B virus; UNG; activation-induced cytidine deaminase; apolipoprotein B mRNA-editing enzyme catalytic subunit; cccDNA; covalently closed circular DNA; differential denaturation DNA PCR; duck hepatitis B virus; uracil-DNA glycosylase

PMID:
23954625
DOI:
10.1016/j.febslet.2013.07.055
[Indexed for MEDLINE]
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