Associations between activation-induced cytidine deaminase/apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like cytidine deaminase expression, hepatitis B virus (HBV) replication and HBV-associated liver disease (Review)

作者：He, Xiuting; Li, Jie; Wu, Jing; Zhang, Manli; Gao, Pujun^*

来源：Molecular Medicine Reports, 2015, 12(5): 6405-6414.

DOI：10.3892/mmr.2015.4312

• hepatitis B virus
• activation-induced cytidine deaminase
• apolipoprotein B mRNA editing enzyme
• catalytic polypeptide-like
• polymorphism
• hepatocellular carcinoma

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-alpha 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.

• 出版日期2015-11
• 单位吉林大学