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The viral capsid antigenic sites of Poliovirus types 1 and 3 are specific structural regions on the exterior of the virus particle, primarily located on the surface loops of the VP1, VP2, and VP3 proteins (Minor, 1990). These sites serve as the primary targets for neutralizing antibodies generated by the host's immune system during natural infection or following immunization (Hogle, 2002). There are several defined antigenic sites (e.g., N-Ag I, II, and III) that vary structurally between serotypes, necessitating the use of multivalent vaccines to ensure broad protection across different poliovirus types (Macadam et al., 1991). Biologically, these sites are involved in the attachment of the virus to the host cell receptor, CD155, and the subsequent conformational changes required for viral uncoating and genome entry (Racaniello, 2006). In therapeutic and prophylactic development, these sites are the focus of Inactivated Poliovirus Vaccines (IPV) and Oral Poliovirus Vaccines (OPV), which induce protective humoral immunity. Additionally, small molecule capsid inhibitors like pocapavir (V-073) target the hydrophobic pocket near these antigenic sites to prevent viral replication by stabilizing the capsid (Collett et al., 2017). Monitoring the genetic stability of these sites is crucial for identifying vaccine-derived polioviruses (VDPVs) that may regain neurovirulence through mutation. Overall, these antigenic determinants are the cornerstone of global polio eradication efforts and the primary interface between the virus and the adaptive immune system.
Induction of neutralizing antibodies that block viral attachment to CD155; stabilization of the viral capsid to prevent genome uncoating; inhibition of viral entry into host cells.
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