Abstract
Chronic hepatitis B affects more than 250 million individuals worldwide, putting them at risk of developing liver cirrhosis and liver cancer. While antiviral immune responses are key to eliminating hepatitis B virus (HBV) infections, insufficient antiviral immunity characterized by failure to eliminate HBV-infected hepatocytes is associated with chronic hepatitis B. Prophylactic vaccination against hepatitis B successfully established protective immunity against infection with the hepatitis B virus and has been instrumental in controlling hepatitis B. However, prophylactic vaccination schemes have not been successful in mounting protective immunity to eliminate HBV infections in patients with chronic hepatitis B. Here, we discuss the current knowledge on the development and efficacy of therapeutic vaccination strategies against chronic hepatitis B with particular emphasis on the pathogenetic understanding of dysfunctional anti-viral immunity. We explore the development of additional immune stimulation measures within tissues, in particular activation of immunogenic myeloid cell populations, and their use for combination with therapeutic vaccination strategies to improve the efficacy of therapeutic vaccination against chronic hepatitis B.
Highlights
More than 250 million individuals suffer from chronic hepatitis B [1], which puts them in danger of developing liver cirrhosis and liver cancer
hepatitis B virus (HBV) infection is observed in some patients with chronic hepatitis B [5], which supports the notion that persistent HBV infection and chronic hepatitis B may be therapeutically targeted by strengthening HBV-specific immunity
These were most often based on novel insights into the immunopathogenesis of HBV infection and novel technologies to improve the strengths of virus-specific immunity
Summary
Hepatitis B Virus (HBV) infection affects almost one-third of the world’s population, and in most cases, is cleared by host anti-viral immunity [1,2]. Liver damage during acute and chronic hepatitis B is caused by the hosts immune response against HBV [2,4] This suggests that a delicate balance exists between mechanisms promoting persistent infection of hepatocytes with HBV and the hosts HBV-specific immune response. Efficient direct antiviral therapies using nucleoside inhibitors are used for treatment in patients with chronic hepatitis B, which inhibit HBV replication but fail to induce protective HBV-specific immunity. Recent studies indicate that expression of these viral an provide a cure from infection with the more pathogenic hepatitis delta virus, which gens in thecoinfection liver rather that secretion of viral antigens and presentation non-hepa requires to replicate, and against which few therapeutic options existon [16]. Immunopathogenesis of HBV Infection and Chronic Viral Hepatitis metabolic microenvironment tolerogenic antigen-presenting cells (Kupffer cells, LSECs, MDSCs)
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