Association of anti-hepatitis B virus pathway with carcinogenesis

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Human APOBEC3 proteins are reported to be antiviral factors and catalyze C-to-U conversion on hepatitis B virus (HBV) DNA by cytosine deamination. Extensive G-to-A hypermutation on plus-strand of HBV DNA has been observed from APOBEC3G-expressing hepatoma cells. We investigated whether UNG also process the hypermutated HBV genome with base excision activity. We found that the UNG inhibition caused accumulation of hypermutation in nuclear cccDNA and decrease of cytoplasmic rcDNA level. Sequencing analysis showed that some of these cccDNA mutations resulted in nonsense codons within viral polymerase coding region. These results suggest that the BER pathway triggered from nuclear UNG repairs the viral DNA mutations introduced by the antiviral APOBECs.