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

被引：13

作者：

Chowdhury, Sajeda ^{[1
]}

Kitamura, Kouichi ^{[1
]}

Simadu, Miyuki ^{[1
]}

Koura, Miki ^{[1
]}

Muramatsu, Masamichi ^{[1
]}

机构：

[1] Kanazawa Univ, Grad Sch Med Sci, Dept Mol Genet, Kanazawa, Ishikawa 9208640, Japan

来源：

FEBS LETTERS | 2013年 / 587卷 / 18期

关键词：

AID; APOBEC; Base excision repair; Hepatitis B virus; cccDNA; HUMAN-IMMUNODEFICIENCY-VIRUS; ROLLING-CIRCLE AMPLIFICATION; CLASS SWITCH RECOMBINATION; APOBEC3G; AID; REPLICATION; INHIBITION; PROTEINS; GENOMES; UNG;

D O I：

10.1016/j.febslet.2013.07.055

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：3148 / 3152

页数：5

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