HBV antigens elicit immune-mediated liver injury in a dose-dependent manner; therefore, low viral antigen load and subsequent resolution of infection in AVH-B as compared to persistent viral antigenemia in chronic HBV infection leads to significantly increased production of HBV specific antibodies (mainly Anti HBe/Anti HBc) in chronic HBV infection or its exacerbation in comparison to AVH-B [559]. This evidence concerns the gene KRT88P and infection.