Published online Oct 21, 2014. doi: 10.3748/wjg.v20.i39.14156
Revised: February 17, 2014
Accepted: April 21, 2014
Published online: October 21, 2014
Chronic hepatitis B (CHB) is a widespread infectious disease with unfavorable outcomes and life-threatening consequences for patients, in spite of modern vaccination and antiviral treatment modalities. Cutting-edge experimental approaches have demonstrated key pathways that involve cross-talk between viral particles and host immune cells. All events, including penetration of hepatitis B virus (HBV) particles into host cells, establishing persistence, and chronization of CHB infection, and possibility of complete elimination of HBV particles are controlled by the immune system. Researchers have paid special attention to the replication capacity of HBV in host cells, which is associated with cellular changes that reflect presentation of viral antigens and variability of HBV antigen features. In addition, specific HBV proteins have an immune-modulating ability to initiate molecular mechanisms that “avoid” control by the immune system. The relationship between immunological shifts and chronic infection stages has been intensively studied since it was recognized that the immune system is a direct participant in the recurrent (cyclic) nature of CHB. Understanding the wide diversity of molecular pathways and the crosstalk between innate and adaptive immune system components will provide fresh insight into CHB immune pathogenesis and the possibilities of developing new treatment strategies for this disease.
Core tip: Chronic hepatitis B (CHB) immunopathogenesis has been comprehensively studied worldwide. Current evidence on the molecular pathways, crosstalk between viral particles and host cells, the role of viral proteins in triggering immune responses, and the content of recruited cells during different stages of viral infection is reviewed aimed at comprehensive analysis and systematization. Concepts concerning the interactions of immune cells in persistent CHB infection have changed, reflecting the possibility of designing new treatment strategies for this disease based on personalized approaches, molecular pathways, and evidence-based criteria.