AI Article Synopsis
- Recent studies indicate that AID plays a role in innate immunity but its exact function in limiting HBV is still not fully understood.
- Overexpressing chicken AID leads to increased mutations and decreased levels of DHBV cccDNA.
- Blocking uracil-DNA glycosylase (UNG) prevents the reduction of cccDNA caused by AID, indicating that the AID/UNG pathway is involved in degrading cccDNA through specific DNA modifications.
Article 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.
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| http://dx.doi.org/10.1016/j.febslet.2013.07.055 | DOI Listing |
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