Published online Sep 6, 2018. doi: 10.12998/wjcc.v6.i9.233
Peer-review started: April 3, 2018
First decision: May 29, 2018
Revised: July 31, 2018
Accepted: August 6, 2018
Article in press: August 7, 2018
Published online: September 6, 2018
The outcomes of hepatitis B virus (HBV) infection are closely related to the age at which infection was acquired. Infection acquired in adult life tends to be self-limited, in contrast to perinatal acquirement, for which chronic persistence of the HBV is a general outcome. Innate immunity plays an indispensable role in early virus infection, facilitating virus clearance. However, it has been reported that HBV is under-recognized and poorly eliminated by the innate immune system in the early stages of infection, possibly explaining the long-lasting persistence of viremia afterwards. Furthermore, due to the existence of covalently closed circular DNA, chronic HBV clearance is very difficult, even when patients are given interferon-α and nucleotide/nucleoside analogs for antiviral therapy. The mechanism by which HBV evades innate immune recognition and establishes persistent infection remains a subject of debate. Besides, some researchers are becoming more interested in how to eradicate chronic HBV infection by restoring or boosting innate immunity. This review aimed to summarize the current knowledge on how intrahepatocyte signaling pathways and innate immune cells act after the onset of HBV infection and how these actions are related to the persistence of HBV. We anticipate the insights presented herein to be helpful for future development of novel immune therapeutic strategies to fight HBV infection.
Core tip: This review covers the following core concepts of hepatitis B virus (HBV) persistence, according to the most up-to-date literature: Hepatocytes lack immune responsiveness to HBV; Innate immune cells display weak responses at the early stages of HBV infection; HBV impairs functions of innate immune cells and select signaling pathways to evade immune recognition and response.