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B-cell receptors (BCRs) and antibodies specific for poliovirus type 1 (PV1) and type 3 (PV3) capsid epitopes are critical components of the adaptive immune system's defense against poliomyelitis (Sutter et al., 2018, Plotkin's Vaccines). These molecules recognize and bind to specific antigenic sites (N-Ag sites) on the viral capsid proteins VP1, VP2, and VP3, which are essential for the virus's ability to infect host cells (Hogle et al., 1985, Science). Upon binding, these antibodies neutralize the virus by blocking its interaction with the human poliovirus receptor (CD155) or by stabilizing the capsid to prevent the release of the viral RNA genome (Minor, 1992, Virology). The induction of these specific BCRs and antibodies is the primary goal of poliovirus vaccination strategies, including the Inactivated Poliovirus Vaccine (IPV) and the Oral Poliovirus Vaccine (OPV) (WHO, 2023). Monitoring the levels and specificity of these antibodies serves as the gold standard for assessing vaccine efficacy and population immunity (CDC, 2021). In therapeutic contexts, monoclonal antibodies targeting these epitopes are being explored as potential treatments or post-exposure prophylaxis, particularly for immunodeficient individuals who may chronically shed the virus (MacLennan et al., 2004, Journal of Infectious Diseases).
Neutralization of viral infectivity by binding to specific capsid epitopes (VP1, VP2, VP3), which sterically hinders viral attachment to the host cell receptor CD155 or prevents the conformational changes required for viral uncoating and genome release (Hogle et al., 1985, Science; Minor, 1992, Virology).
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