Chronic hepatitis B (CHB) is a life-threatening liver disease affecting 257 million people worldwide, in particular in the Asia-Pacific regions. In endemic areas, hepatitis B virus (HBV) is usually transmitted from chronically infected mothers to neonates. Perinatal HBV infection causes chronic infection in more than 90% of exposed individuals. With perinatal infection, lifetime mortality risk due to complications of liver cirrhosis (LC) or hepatocellular carcinoma (HCC) reaches up to 40% in men and 15% in women.
For the treatment of chronic HBV infection, nucleos(t)ide analogue antivirals have been successfully used to suppress viral replication. However, HBV exists as a cccDNA, which cannot be eliminated by nucleos(t)ide analogues. Therefore, a practical goal of novel HBV therapeutics can be HBs seroconversion (loss of HBsAg and development of HBsAg-specific antibodies), which occurs during spontaneous recovery from acute HBV infection. This HBs seroconversion is referred to as “functional cure” of HBV infection. When functional cure is reached, HBsAg-specific antibodies have virus-neutralizing activity and control HBV infection even in the presence of cccDNA. Currently, peg-IFN-a is often used to induce HBs seroconversion in patients with chronic HBV infection; however, the efficacy is not satisfactory. In future, other immunological therapeutics must be considered to achieve HBs seroconversion, including therapeutic vaccines and immune checkpoint blockers.
This Research Topic covers the mechanisms of immune dysfunction in chronic HBV infection and novel therapeutic approaches to overcome it. We welcome the submission of Original Research articles, Case Report, Review, Opinion, Perspective, Systematic Review, and Correction which cover the following topics:
1. Mechanisms of dysfunctional Innate and adaptive immune response in chronic HBV infection (interferon and cytokine response, T cell response, NK cell response, B cell response, NKT cell response, regulatory T cells and myeloid-derived suppressor cells, monocyte and macrophages)
2. Ways to overcome immune dysfunction – boosting interferon response
3. Ways to overcome immune dysfunction – boosting T & NK cell response
4. Ways to overcome immune dysfunction – various therapeutic vaccines
5. Ways to overcome immune dysfunction – immune checkpoint blockers
Chronic hepatitis B (CHB) is a life-threatening liver disease affecting 257 million people worldwide, in particular in the Asia-Pacific regions. In endemic areas, hepatitis B virus (HBV) is usually transmitted from chronically infected mothers to neonates. Perinatal HBV infection causes chronic infection in more than 90% of exposed individuals. With perinatal infection, lifetime mortality risk due to complications of liver cirrhosis (LC) or hepatocellular carcinoma (HCC) reaches up to 40% in men and 15% in women.
For the treatment of chronic HBV infection, nucleos(t)ide analogue antivirals have been successfully used to suppress viral replication. However, HBV exists as a cccDNA, which cannot be eliminated by nucleos(t)ide analogues. Therefore, a practical goal of novel HBV therapeutics can be HBs seroconversion (loss of HBsAg and development of HBsAg-specific antibodies), which occurs during spontaneous recovery from acute HBV infection. This HBs seroconversion is referred to as “functional cure” of HBV infection. When functional cure is reached, HBsAg-specific antibodies have virus-neutralizing activity and control HBV infection even in the presence of cccDNA. Currently, peg-IFN-a is often used to induce HBs seroconversion in patients with chronic HBV infection; however, the efficacy is not satisfactory. In future, other immunological therapeutics must be considered to achieve HBs seroconversion, including therapeutic vaccines and immune checkpoint blockers.
This Research Topic covers the mechanisms of immune dysfunction in chronic HBV infection and novel therapeutic approaches to overcome it. We welcome the submission of Original Research articles, Case Report, Review, Opinion, Perspective, Systematic Review, and Correction which cover the following topics:
1. Mechanisms of dysfunctional Innate and adaptive immune response in chronic HBV infection (interferon and cytokine response, T cell response, NK cell response, B cell response, NKT cell response, regulatory T cells and myeloid-derived suppressor cells, monocyte and macrophages)
2. Ways to overcome immune dysfunction – boosting interferon response
3. Ways to overcome immune dysfunction – boosting T & NK cell response
4. Ways to overcome immune dysfunction – various therapeutic vaccines
5. Ways to overcome immune dysfunction – immune checkpoint blockers