Publications by authors named "Miyuki Simadu"
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.
The covalently closed circular DNA (cccDNA) of the hepatitis B virus (HBV) plays an essential role in chronic hepatitis. The cellular repair system is proposed to convert cytoplasmic nucleocapsid (NC) DNA (partially double-stranded DNA) into cccDNA in the nucleus. Recently, antiviral cytidine deaminases, AID/APOBEC proteins, were shown to generate uracil residues in the NC-DNA through deamination, resulting in cytidine-to-uracil (C-to-U) hypermutation of the viral genome.
View Article and Find Full Text PDF