B-cell receptor specific for Varicella-Zoster Virus (VZV) glycoprotein E (gE)

B-cell receptors specific for Varicella-Zoster Virus (VZV) glycoprotein E (gE) are membrane-bound immunoglobulins on B lymphocytes that selectively recognize the gE antigen, the most prevalent and immunogenic surface protein of VZV (PubMed: 25122792). These receptors play a pivotal role in the adaptive immune response by capturing the viral antigen and initiating intracellular signaling pathways that lead to B-cell activation and differentiation (Janeway's Immunobiology). Glycoprotein E itself is indispensable for VZV infectivity, facilitating viral entry and cell-to-cell transmission (PubMed: 11832479). In the context of pharmacology, these BCRs are the primary targets for recombinant vaccines like Shingrix, which present purified gE to the immune system to elicit a protective response (FDA). Upon binding, the BCRs trigger the production of neutralizing antibodies that prevent the virus from infecting new cells and help maintain latency, thereby preventing shingles (StatPearls: Herpes Zoster). Understanding the interaction between gE and its specific BCRs is crucial for developing next-generation immunotherapies and monitoring vaccine efficacy in aging populations (PubMed: 29443654).

Other names

VZV gE-specific B-cell receptorAnti-VZV glycoprotein E BCRVaricella-Zoster Virus gE-specific BCRAnti-gE B-cell receptor

Antigen-mediated activation of the B-cell receptor triggers intracellular signaling through the CD79a/CD79b heterodimer, leading to B-cell proliferation, affinity maturation, and differentiation into plasma cells that secrete neutralizing antibodies against VZV gE.