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Sabin poliovirus type 1 is a live-attenuated strain of Poliovirus type 1, originally developed by Albert Sabin for use in the Oral Poliovirus Vaccine (OPV) [5, 19]. It was derived from the neurovirulent Mahoney strain through extensive serial passage in non-human primate cells, resulting in specific mutations—particularly within the 5' untranslated region (UTR) and capsid proteins—that significantly reduce its ability to infect the central nervous system [2, 6, 12]. The virus functions by entering host cells via the CD155 receptor and utilizing an internal ribosome entry site (IRES) to initiate the translation of its RNA genome [2, 7]. In a clinical context, it is used to induce robust mucosal and systemic immunity, providing protection against wild-type poliovirus infection [8, 9]. However, a major therapeutic challenge is the rare occurrence of genetic reversion, where the attenuated virus regains neurovirulence, potentially causing vaccine-associated paralytic poliomyelitis (VAPP) or giving rise to circulating vaccine-derived polioviruses (cVDPV) [3, 15]. Consequently, global health strategies are transitioning toward the use of Sabin-strain Inactivated Poliovirus Vaccines (sIPV) to mitigate these risks while maintaining population immunity [13, 14]. Monitoring neutralizing antibody titers and viral shedding remains critical for assessing vaccine efficacy and safety in global eradication efforts [3, 19].
Induction of mucosal and systemic neutralizing antibodies (IgA and IgG); viral capsid binding and inhibition of uncoating (for antivirals).
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