Published online Jun 16, 2022. doi: 10.12998/wjcc.v10.i17.5518
Peer-review started: January 5, 2022
First decision: January 27, 2022
Revised: January 30, 2022
Accepted: April 4, 2022
Article in press: April 4, 2022
Published online: June 16, 2022
Processing time: 154 Days and 23.4 Hours
With over 40 years of history, occult hepatitis B infection (OBI) continues to remain an important and challenging public health problem. Defined as the presence of replication-competent hepatitis B virus (HBV) DNA (i.e., episomal HBV covalently closed circular DNA) in the liver and/or HBV DNA in the blood of people who test negative for hepatitis B surface antigen (HBsAg) in currently available assays, OBI is currently diagnosed using polymerase chain reaction (PCR) and real-time PCR assays. However, all efforts should be made to exclude a false negative HBsAg in order to completely follow the definition of OBI. In recent years, significant advances have been made in understanding the HBV lifecycle and the molecular mechanisms that lead to the persistence of the virus in the occult form. These factors are mainly related to the host immune system and, to a smaller proportion, to the virus. Both innate and adaptive immune responses are important in HBV infection management, and epigenetic changes driven by host mechanisms (acetylation, methylation, and microRNA implication) are added to such actions. Although greater genetic variability in the S gene of HBV isolated from OBIs was found compared with overt infection, the mechanisms of OBI are not mainly viral mutations.
Core Tip: Every year, our knowledge of occult hepatitis B infection becomes richer with new information. This review is an up-to-date analysis of the viral and host factors that interact and lead to an occult form of hepatitis B virus infection. The latest discoveries in microRNA involvement, epigenetic mechanisms, immune system factors, and viral variants have been included for a comprehensive understanding of this challenging problem. We emphasize that occult hepatitis B infection is not only and not primarily a virus-driven condition; host immune and epigenetic mechanisms are also its important determinants.