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Literature DB >> 23954625

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

Sajeda Chowdhury¹, Kouichi Kitamura, Miyuki Simadu, Miki Koura, Masamichi Muramatsu.

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.

Entities: Chemical Gene Species

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

Mesh：

Substances：

Year: 2013 PMID： 23954625 DOI： 10.1016/j.febslet.2013.07.055

Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124

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Cited

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