The hepatitis B virus (HBV) infection is a major risk factor in the development of chronic hepatitis (CH) and hepatocellular carcinoma (HCC). The activation‑induced cytidine deaminase (AID)/apolipoprotein B mRNA editing enzyme, catalytic polypeptide‑like (APOBEC) family of cytidine deaminases is significant in innate immunity, as it restricts numerous viruses, including HBV, through hypermutation‑dependent and ‑independent mechanisms. It is important to induce covalently closed circular (ccc)DNA degradation by interferon‑α without causing side effects in the infected host cell. Furthermore, organisms possess multiple mechanisms to regulate the expression of AID/APOBECs, control their enzymatic activity and restrict their access to DNA or RNA substrates. Therefore, the AID/APOBECs present promising targets for preventing and treating viral infections. In addition, gene polymorphisms of the AID/APOBEC family may alter host susceptibility to HBV acquisition and CH disease progression. Through G‑to‑A hypermutation, AID/APOBECs also edit HBV DNA and facilitate the mutation of HBV DNA, which may assist the virus to evolve and potentially escape from the immune responses. The AID/APOBEC family and their associated editing patterns may also exert oncogenic activity. Understanding the effects of cytidine deaminases in CH virus-induced hepatocarcinogenesis may aid with developing efficient prophylactic and therapeutic strategies against HCC.