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Poliovirus type 2 (PV2) antigens refer to the structural proteins that comprise the viral capsid, specifically VP1, VP2, VP3, and VP4. These proteins are organized in an icosahedral arrangement and are responsible for protecting the viral RNA genome, facilitating host cell attachment via the CD155 (PVR) receptor, and mediating the uncoating process required for viral entry. As antigens, they are the primary targets of the humoral immune response, serving as the functional components of the Inactivated Poliovirus Vaccine (IPV) and the Oral Poliovirus Vaccine (OPV). Neutralizing antibodies directed against these capsid proteins prevent the virus from infecting motor neurons and causing poliomyelitis. In addition to their role in immunization, these antigens are the focus of therapeutic drug development. Small-molecule capsid inhibitors, such as V-073 and pleconaril, target the hydrophobic pocket of the VP1 protein to stabilize the capsid and block the conformational changes necessary for viral uncoating. While wild-type poliovirus type 2 was declared eradicated in 2015, the antigens remain critical due to the emergence of vaccine-derived poliovirus strains (cVDPV2). Modern strategies include the use of novel OPV2 (nOPV2), which utilizes modified PV2 antigens with improved genetic stability to reduce the risk of reversion to neurovirulence while maintaining strong immunogenicity.
Induction of neutralizing antibodies against viral capsid proteins to prevent infection (vaccines); binding to the hydrophobic pocket of the VP1 capsid protein to inhibit viral uncoating and RNA release (antivirals).
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