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Sabin poliovirus type 3 is a live-attenuated strain of the poliovirus serotype 3, which serves as a critical component of the oral poliovirus vaccine (OPV) and is used in the production of Sabin-strain inactivated poliovirus vaccines (sIPV) [2, 4]. It was developed by Albert Sabin through the attenuation of the neurovirulent Leon 12a1b strain, involving key genetic modifications such as the U-to-C mutation at nucleotide 472 in the 5' untranslated region (UTR) [13, 14]. As a member of the Picornaviridae family, it is a non-enveloped virus with a positive-sense single-stranded RNA genome that encodes a polyprotein subsequently cleaved into structural (VP1-VP4) and non-structural (2A-3D) proteins [12, 14]. The virus infects host cells by binding to the poliovirus receptor (CD155) and replicates primarily in the gastrointestinal tract, inducing both mucosal and systemic immunity [2, 17]. However, Sabin type 3 is the most genetically unstable of the Sabin strains, with a high propensity to revert to a neurovirulent phenotype, which can cause vaccine-associated paralytic poliomyelitis (VAPP) or lead to the emergence of circulating vaccine-derived polioviruses (cVDPV3) [8, 13]. Therapeutic agents targeting the virus include capsid-binding inhibitors like pocapavir (V-073) and pleconaril, which block viral uncoating, as well as the nucleoside analog ribavirin, which acts as a mutagen to inhibit viral replication [1, 12].
Capsid binding, inhibition of viral uncoating, and inhibition of viral RNA-dependent RNA polymerase.
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