Figure 2.

Role of the hepatitis B surface protein in the immune response to hepatitis B infection. Hepatitis B virus (HBV) primary infection does not induce activation of intracellular antiviral mechanisms through transcription of interferon inducible genes. After acute infection, the evolution to resolved hepatitis B is promoted by a vigorous and multispecific T cell response (CD4+ and CD8+ T cell) through hepatocyte apoptosis and interferon (IFN)-γ secretion, while evolution to chronicity is characterized by a weak and focused T cell response. Regulatory T cells (Treg) cells (LT REG) limit the function of effector T cells preventing excessive auto-destructive disease. A protective immunity is due in part to humoral and cellular anti-envelope response, preventing HBV attachment to hepatocytes, thus playing a critical role in prevention of infection after classical vaccination and in viral clearance in resolved hepatitis. HLA: Human leukocyte antigen.