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Hepatitis B is a major global health burden caused by the HBV. Infection with HBV induces a necro-inflammatory liver disease and can either be self-limiting or persisting. Persisting or more precisely chronic HBV infection can progress to liver cirrhosis, end-stage liver disease and even liver cancer and thus results in an increased risk of dying prematurely. An effective and safe vaccine is available that confers over 95% protection by eliciting an immune response against the surface antigen of HBV (HBsAg). Indeed, a protective adaptive memory response mediated by memory T cells, memory B cells and anti-HBsAg antibodies is detectable on Hepatitis B vaccination.1
Generally, current vaccination strategies target the adaptive arm of the immune system exploiting its capacity to establish a long-lasting protective immunological memory. However, it is becoming increasingly clear that not only the adaptive immune cells, the B and T cells, adapt their function on pathogen encounter to mediate protection on reinfection but also the innate immune system is able to establish a memory state that is called ‘trained immunity’ or ‘innate memory’.2 For example, natural killer (NK) cells are innate cytotoxic lymphocytes that are important in the early immune response towards viral infections and can mediate trained rather unspecific immunity or even specific innate immune memory responses on re-challenge.3 However, only very …