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Poliovirus type 1 (PV1) is a highly infectious human pathogen belonging to the Picornaviridae family and is the primary cause of paralytic poliomyelitis (NIH, Abcam). The viral target is an icosahedral capsid composed of 60 repeating units of four structural proteins: VP1, VP2, VP3, and VP4 (NIH). These proteins are responsible for protecting the viral RNA genome and facilitating attachment to the host cell receptor, CD155 (PVR) (Abcam, NIH). Upon binding to CD155, the capsid undergoes conformational changes that lead to the release of the viral genome into the host cytoplasm, a process known as uncoating (NIH). Monoclonal antibodies against PV1 typically target epitopes on the capsid surface, such as the canyon region, to neutralize the virus by blocking receptor interaction (NIH, PNAS). Small-molecule antivirals, such as pleconaril and pocapavir, also target the capsid by binding to a hydrophobic pocket in VP1, thereby stabilizing the structure and preventing uncoating (NIH). PV1 is the most prevalent and virulent of the three poliovirus serotypes, making its capsid a critical target for both vaccine development and therapeutic intervention (NIH). Passive immunization using monoclonal antibodies is being explored as a strategy to support the global polio eradication initiative, particularly for treating persistent infections in immunodeficient individuals (NIBSC, PNAS).
Capsid stabilization and inhibition of viral uncoating (NIH); blocking of viral attachment to the CD155 receptor (NIH, PNAS).
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