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Distribution and difference of APOBEC‐induced mutations in the TpCpW context of HBV DNA between HCC and non‐HCC

Hepatitis B virus (HBV) DNA is vulnerable to editing by human apolipoprotein B mRNA editing enzyme, catalytic polypeptide‐like (APOBEC) cytidine deaminases. However, the distribution of APOBEC‐induced mutations on HBV DNA is not well characterized. To this end, we obtained the HBV DNA sequence of HBV‐infected individuals with and without hepatocellular carcinoma (HCC and non‐HCC groups, respectively) from NCBI database and calculated the rapo values of APOBEC‐induced TpCpW→TpKpW mutation prevalence in HBV DNA. The results showed that the APOBEC‐induced mutations were mainly distributed in the minus strand of non‐HCC‐derived HBV DNA (rapo = 2.04), while the mutation on the plus‐strand was weaker (rapo = 0.99). There were high APOBEC‐induced mutation regions in the minus strand of HBV DNA 1 to 1000 nucleotides (nts) region and in the plus‐strand of HBV DNA 1000 to 1500 nts region; the mutations in the 1 to 1000 nts region were mainly TpCpW→TpTpW mutation types (total T/G: 111/18) and a number of these were missense mutations (missense/synonymous: 35/94 in P gene, 17/15 in S gene, and 5/10 in X gene). The difference between minus to plus‐strand rapo of HCC‐derived HBV DNA (1.96) was greater than that of the non‐HCC group (1.05). The minus‐strand rapo of HCC‐derived HBV DNA regions 1000 to1500nts and 1500 to 2000 nts (rapo = 4.2 and 4.2) was also higher than that of the same regions of non‐HCC‐derived HBV DNA (rapo = 1.2 and 1.1). Finally, the ratio of minus to plus‐strand rapo was used to distinguish HCC‐derived HBV DNA from non‐HCC‐derived HBV DNA. This study unraveled the distribution characteristics of APOBEC‐induced mutations on double strands of HBV DNA from HCC and non‐HCC samples. Our findings would help understand the mechanism of APOBECs on HBV DNA and may provide important insights for the screening of HCC.