Pathogenesis of Hepatitis B

Eradication of HBV infection depends on the coordinate and efficient development of humoral and cell-mediated immune responses against HBV proteins. Antibodies secreted by plasma cells (PC) derived from antigen-specific B cells (which usually recognize viral antigens in their native conformation) are mostly responsible for the neutralization of free circulating viral particles, Cytotoxic T cells (CTL) that recognize endogenous viral antigens in the form of short peptides associated with human leukocyte antigen (HLA) class I molecules on the surface of the infected hepatocytes (HC) are the main effectors for the elimination of intracellular virus. They can do this by at least two different mechanisms: direct attachment to the cell membrane, causing the infected cell to undergo apoptosis; and the release of soluble cytokines that can downregulate viral gene expression, leading to the elimination of intracellular virus without destruction of the infected cell. Both humoral and cytotoxic functions are more or less stringently regulated by the helper effect of the CD4+ T cells (TH) that recognize exogenous viral antigens, released or secreted by liver cells, in the form of short peptides that associate with HLA class II molecules in the endosomal compartment of professional antigen-presenting cells such as B cells, macrophages (Mø), and dendritic cells.