Recently, Professor Ma Chunhong's team of the school of Basic Medicine published a research paper entitled "hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1 mediated virtual RNAs editing in hepatecytes" online in the journal Cellular & Molecular Immunology (CAS-1, 2020, if = 11.5), Wang Liyuan, a doctoral student of the school of basic medicine, is the first author of the paper. Professor Ma Chunhong and associate researcher Wu Zhuanchang of Shandong University are the co-corresponding authors of the paper. Shandong University is the independent first and corresponding author unit of the paper.

RNA-specific adenosine deaminase (ADAR1) can catalyze the deamination of adenosine (A) into inosine (I) in double-stranded RNA, thus changing the secondary structure of RNA, which is an important mechanism for the host to distinguish self from non-self RNAs. In this study, we found that ADAR1 binds to and edits HBVRNAs and inhibits the binding of the pattern-recognition receptor RIG-I/MDA5 to HBVRNAs, thereby negatively regulating IFN signaling pathway activation and promoting HBV replication. HBV X protein transactivates ADAR1 transcription through transcription factor YY1, upregulates immune recognition threshold, and promotes HBV to evade host immune recognition. Intervention of ADAR1 can effectively enhance liver immune function and promote HBV clearance. This study reveals the molecular mechanism by which HBV hijacks ADAR1 to promote viral immune escape, providing a theoretical basis for the development of more effective HBV treatment strategies.

Paper link: https://www.nature.com/articles/s41423-021-00729-1