Published online Oct 28, 2022. doi: 10.3748/wjg.v28.i40.5784
Peer-review started: May 10, 2022
First decision: August 20, 2022
Revised: September 8, 2022
Accepted: October 9, 2022
Article in press: October 9, 2022
Published online: October 28, 2022
Processing time: 170 Days and 23.3 Hours
Hepatitis B virus (HBV) infection is a global public health issue. Interferon-α (IFN-α) treatment has been used to treat hepatitis B for over 20 years, but fewer than 5% of Asians receiving IFN-α treatment achieve functional cure. Thus, IFN-α retreatment has been introduced to enhance antiviral function. In recent years, immune-related studies have found that the complex interactions between immune cells and cytokines could modulate immune response networks, in-cluding both innate and adaptive immunity, triggering immune responses that control HBV replication. However, heterogeneity of the immune system to control HBV infection, particularly HBV-specific CD8+ T cell heterogeneity, has consequ-ential effects on T cell-based immunotherapy for treating HBV infection. Altogether, the host’s genetic variants, negative-feedback regulators and HBV components affecting the immune system's ability to control HBV. In this study, we reviewed the literature on potential immune mechanisms affecting the im
Core Tip: Hepatitis B virus (HBV)-specific immune control is characterized by distinct phenotypical and functional profiles. Owing to the negative feedback associated with all immune responses in an infected host, immunomodulators regulating a single immune pathway are unlikely to fully restore antiviral immunity. Interferon-α (IFN-α) treatment was shown to simultaneously affect multiple immune pathways and various immune cell populations in the host and integrate signals toward improving HBV-specific immune control. In addition, IFN-α retreatment was shown to improved functional cure rates, indicating that could gradually enhance the overall immune control.