About this Research Topic
There are still about 257 million individuals worldwide living with chronic Hepatitis B Virus (HBV) infection, which are at high risk of liver cirrhosis, liver failure and liver cancer, which account for the majority of end-stage liver diseases. The dysfunctional immune responses play an essential role in persistent HBV infection and liver inflammation. Immune responses during chronic hepatitis B are characterized by 1) dysfunctions and exhaustion of HBV-specific CD4 and CD8 T cells, 2) decreased amount and dysfunction of DCs and NKs/NKTs, 3) up-regulated/enhanced expression of regulatory factors, including the immune checkpoint proteins PD-1, CTLA-4, and Tim-3, and 4) impaired innate immune response, especially TLRs downregulation and dysfunction. Thus, modulating the host immune system to strengthen specific cellular immune reactions might help eliminate HBV. Strategies restoring/enhancing innate immunity and inducing HBV-specific adaptive immune responses have been tested in preclinical and clinical trials, with attractive effects. However, the molecular mechanisms accounting for HBV persistence are not fully elucidated, and the progress in basic research will facilitate the immunomodulatory strategies for curing chronic HBV infection.
This Research Topic aims at reporting the latest advances in targeting the immune system to treat HBV infection from both basic and clinical perspectives. We welcome submissions of Original Research, Review and Mini Review on the subtopics below:
- The role of immune system accounting for HBV persistence and clearance, especially the vital role of T and B cells and antibody responses.
- The cross talk between the immune system and HBV in various stages.
- The dysfunction of innate immune system in chronic HBV infection.
- The functional status of adaptive immune responses in chronic HBV infection.
- The host factors affecting the immune control of HBV.
- The impact of viral genetic variability in modulating HBV-specific immune responses.
- Strategies to manipulate innate immunity (TLR, RIG I, STING) to establish an antiviral state.
- Strategies of HBV-specific immunotherapy (Novel vaccine, TCR-T/CAR-T, PD-1/PD-L1 antibodies).
Topic Editor Anna D. Kosinska is listed as inventor of a patent application describing the scheme of therapeutic hepatitis B vaccine TherVacB (PCT/EP2017/050553). The other Topic Editors declare no conflict of interest with regards to the Research Topic theme.
This Research Topic aims at reporting the latest advances in targeting the immune system to treat HBV infection from both basic and clinical perspectives. We welcome submissions of Original Research, Review and Mini Review on the subtopics below:
- The role of immune system accounting for HBV persistence and clearance, especially the vital role of T and B cells and antibody responses.
- The cross talk between the immune system and HBV in various stages.
- The dysfunction of innate immune system in chronic HBV infection.
- The functional status of adaptive immune responses in chronic HBV infection.
- The host factors affecting the immune control of HBV.
- The impact of viral genetic variability in modulating HBV-specific immune responses.
- Strategies to manipulate innate immunity (TLR, RIG I, STING) to establish an antiviral state.
- Strategies of HBV-specific immunotherapy (Novel vaccine, TCR-T/CAR-T, PD-1/PD-L1 antibodies).
Topic Editor Anna D. Kosinska is listed as inventor of a patent application describing the scheme of therapeutic hepatitis B vaccine TherVacB (PCT/EP2017/050553). The other Topic Editors declare no conflict of interest with regards to the Research Topic theme.
Keywords: Hepatitis B Virus, Immune response, Immune tolerance, Immunotherapy, T cell therapy, Innate immunity, Therapeutic vaccine
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
