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Sabin poliovirus type 2 is a live-attenuated strain of the Type 2 poliovirus, a member of the Enterovirus C species within the Picornaviridae family [World Health Organization, 2023]. It was developed by Albert Sabin through repeated passage in non-human cells, resulting in specific mutations in the 5' untranslated region (UTR) and the capsid proteins that significantly reduce its neurovirulence and replication efficiency in the human gut compared to wild-type strains [Kew et al., 2002]. As a therapeutic target, it is the primary component of the Type 2 oral poliovirus vaccine (OPV2) and the novel oral poliovirus vaccine type 2 (nOPV2), which are designed to elicit both systemic and mucosal immunity to prevent poliomyelitis [Van Damme et al., 2019]. However, the genetic instability of the Sabin 2 strain allows it to occasionally revert to a pathogenic state, causing vaccine-associated paralytic poliomyelitis (VAPP) or circulating vaccine-derived polioviruses (cVDPV2) [Macklin et al., 2020]. Antiviral agents such as pocapavir target the viral capsid of Sabin 2 to inhibit the uncoating process, providing a potential treatment for chronic shedders or as an adjunct in eradication efforts [Collett et al., 2017].
Vaccines (OPV2, nOPV2, IPV) function by presenting viral antigens to the immune system, inducing the production of neutralizing antibodies (IgG and secretory IgA) that bind to the viral capsid and prevent infection [World Health Organization, 2023; Van Damme et al., 2019]. Antiviral agents like pocapavir act as capsid inhibitors; they bind to a hydrophobic pocket within the VP1 protein of the viral capsid, which stabilizes the structure and prevents the conformational changes necessary for the virus to release its RNA genome into the host cell [Collett et al., 2017; Macklin et al., 2020].
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