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B-cell receptors (BCRs) specific for varicella-zoster virus (VZV) glycoproteins are membrane-bound immunoglobulins expressed on the surface of B lymphocytes that recognize and bind to specific viral surface proteins, most notably glycoprotein E (gE), gB, and the gH/gL complex (PMID: 25101571). These receptors are fundamental to the adaptive immune response against VZV, the pathogen responsible for varicella (chickenpox) and herpes zoster (shingles) (PMID: 20686019). Upon binding to their cognate viral glycoproteins, these BCRs initiate intracellular signaling cascades that lead to B-cell activation, clonal expansion, and differentiation into antibody-secreting plasma cells and long-lived memory B cells (PMID: 29445124). In clinical practice, these receptors are the primary targets of vaccination strategies; for example, the recombinant zoster vaccine (Shingrix) utilizes a truncated gE protein to specifically stimulate these BCRs and elicit a potent, durable immune response in older adults (PMID: 25916341). Additionally, passive immunization with VZV-specific immunoglobulins (VariZIG) provides immediate protection by mimicking the binding specificity of these receptors to neutralize the virus in high-risk individuals (CDC, 2013).
Vaccines (e.g., Shingrix, Varivax) act as antigenic agonists that bind to and activate these B-cell receptors, triggering B-cell differentiation into memory cells and plasma cells (PMID: 25916341). Passive immunotherapies (e.g., VariZIG) provide exogenous antibodies that mimic the binding specificity of these BCRs to neutralize VZV glycoproteins and prevent viral entry into host cells (PMID: 29445124).
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