Abstract
The clinical sequelae associated with chronic HBV infection is generally regarded as a consequence of an inadequate and inappropriate immune response to active viral replication, predominantly at the T-cell level. However, recent studies on hepatitis B surface antigen (HBsAg)-specific B cells and hepatitis B surface antibody (anti-HB) responses have identified their previously unrecognized role in the pathogenesis of chronic hepatitis B (CHB). These studies have also uncovered novel therapeutic approaches to more effectively target HBsAg loss and seroconversion, an important end point and regarded as a functional cure. Anti-HBs IgG has also been shown to have multiple direct acting antiviral roles with the Fab component directly blocking viral entry, and release while the Fc component has been linked to antibody dependent cellular cytotoxicity. Likewise, the HBsAg-specific B-cell dysfunctionality can be reversed providing new therapeutic opportunities to achieve functional cure in CHB.
Highlights
A co-ordinated adaptive immune response of both B cells and T cells are required to achieve virus clearance in acute HBV infection. Dysfunction of both T-cell and B-cell responses have been observed during chronic hepatitis B infection
HBsAg-specific B cells in chronic hepatitis B patients are accumulated in exhausted phenotype and are defect of differentiating into antibody producing cells
Immune complexes of anti-HBs with HBsAg and co-existing anti-HBs and HBsAg have been observed in chronic hepatitis B infected patients, their relative function remains elusive
Summary
A co-ordinated adaptive immune response of both B cells and T cells are required to achieve virus clearance in acute HBV infection. Dysfunction of both T-cell and B-cell responses have been observed during chronic hepatitis B infection. Anti-HBs can block entry of virus, assembly of subviral particles and secretion/release of subviral particles, induce antibody-dependent cell cytotoxicity of infected cells.
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