IMMUNE-MECHANISMS UNDERLYING HBV PERSISTENCE

Recent developments in our understanding of molecular mechanisms underlying T cell growth and differentiation have helped to identify previously unknown variables in the host response against virally infected targets. While recognition of viral proteins in HLA-association provides an initial triggering signal for pre-effector cell activation the functional outcome of an immune response is dependent on additional costimulatory signals that are mediated through a set of accessory receptors exposed in the T cell plasma membrane. Availability of such costimulatory signals decides whether T cells will develop into effector cells capable of viral elimination or, alternatively, whether specific tolerance is induced. One important parameter contributing to viral persistence and chronic disease following HBV-infection are secondary immunodeficiencies which mainly exist at the level of accessory receptor stimulation. The elucidation of the molecular basis of acquired immunodeficiencies provides novel perspectives for rational immune reconstitution and efficient antiviral immunity.