Hepatitis A virus-specific B-cell receptor (HAV-specific BCR)

The B-cell receptor (BCR) specific for hepatitis A virus (HAV) capsid epitopes is a membrane-bound immunoglobulin complex that plays a central role in the adaptive immune response to HAV. These receptors are expressed on the surface of HAV-specific B cells and are responsible for recognizing and binding to neutralizing epitopes on the viral capsid, particularly those involving the VP1, VP2, and VP3 proteins (Wang et al., 1996; Wang et al., 2015). Upon antigen binding, the BCR triggers intracellular signaling cascades that lead to B-cell activation, proliferation, and differentiation into plasma cells that secrete high-affinity neutralizing antibodies (Lemon et al., 2017). These antibodies, primarily of the IgM and IgG isotypes, provide protection by blocking viral attachment to host cell receptors or by interfering with the uncoating process (Cao et al., 2019). Inactivated HAV vaccines, such as Havrix and Vaqta, function by presenting these capsid epitopes to the BCR, thereby inducing long-lasting protective immunity (CDC, 2024). The characterization of these receptors and their corresponding epitopes is crucial for the development of both vaccines and monoclonal antibody-based therapies for post-exposure prophylaxis (Wang et al., 2015). Understanding the repertoire of these receptors is also vital for monitoring vaccine efficacy and identifying potential escape mutants.

Other names

Anti-HAV B-cell receptorHepatitis A virus capsid-specific BCRHAV-specific BCRHepatitis A virus-specific immunoglobulin receptor

Vaccine-derived viral capsid epitopes bind to the HAV-specific B-cell receptor, initiating signal transduction that leads to B-cell activation, clonal expansion, and the production of neutralizing antibodies that prevent viral infection.