Human hepatitis B virus (HBV) infects the liver of humans or humanoid primates. In humans, HBV infection often causes an inflammatory liver disease - hepatitis B. The virus is transmitted by perinatal, percutaneous and sexual exposure, as well as by close person-to-person contact. The latter occurs especially among young children, presumably by open cuts or sores. Vertical transmission from mothers to their neonates, or infection during the first year of life, results in persistent often lifelong infection in >90% of cases. In contrast, infection during adulthood is cleared in >95% of cases, and results in lifelong protective immunity. While a correlation between the strength of HBV-specific T cell responses and virus clearance has been established, factors determining the strength of a T cell response as well as factors shifting the balance from immune tolerance to immune clearance are hardly understood. The innate immune response, early adaptive B and T cell responses, regulatory T cells, the liver microenvironment, and the peculiar properties of hepatocytes and nonparenchymal liver cells to present antigen seem to play a role. Understanding this complex interplay requires systematic immune monitoring of well characterized human cohorts, but also experimental approaches using primary human cells and genetically modified mouse models. Using these models, we begin to understand the immune recognition of HBV and how it influences the outcome of HBV infection. In this paper we review the current knowledge about virus-host interactions and how it influences the outcome of HBV infection and describe the immune signatures associated with clinical recovery and/or persistent infection.