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Human adaptive immune receptors recognizing inactivated poliovirus type 2 (IPV2) capsid antigens comprise the B-cell receptors (BCRs) and T-cell receptors (TCRs) that specifically bind to the structural proteins of the poliovirus type 2 shell (PubMed: 28235240). These receptors are the primary mediators of the protective immune response elicited by the Salk-type inactivated poliovirus vaccine (CDC, 2023). The poliovirus capsid is composed of four proteins (VP1, VP2, VP3, and VP4), with VP1 containing the most critical epitopes for virus neutralization (UniProt: P03300). Upon vaccination, these receptors facilitate the generation of high-affinity neutralizing antibodies, primarily of the IgG isotype, which circulate systemically to prevent the virus from infecting the central nervous system. This target is essential for maintaining population immunity against the type 2 serotype, which was declared eradicated in its wild form but continues to pose a threat through circulating vaccine-derived strains (WHO, 2022). The interaction between these receptors and the inactivated antigens leads to the formation of long-lived immunological memory, providing durable protection against paralytic poliomyelitis (PubMed: 31501135).
The mechanism involves the recognition of specific D-antigen epitopes on the inactivated poliovirus type 2 capsid (VP1, VP2, and VP3) by B-cell receptors, which triggers clonal expansion and the secretion of neutralizing antibodies (PubMed: 26903200). These antibodies bind to the viral capsid and sterically hinder the virus's ability to attach to the host cell receptor, CD155, thereby preventing viral entry and replication (PubMed: 28235240).
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