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Poliovirus type 1 (PV1) is a small, non-enveloped virus with a positive-sense single-stranded RNA genome, belonging to the Enterovirus genus of the Picornaviridae family [1, 2]. It is the primary causative agent of poliomyelitis, a disease that can lead to irreversible paralysis by destroying motor neurons in the central nervous system [5, 9]. The virus enters host cells by binding to the CD155 receptor, after which it hijacks the cellular machinery to replicate its genome and produce viral proteins through an IRES-mediated translation process [2, 8]. Therapeutic intervention primarily involves vaccination with inactivated (IPV) or live-attenuated (OPV) strains to induce protective neutralizing antibodies [4, 12]. Additionally, experimental antiviral drugs like Pocapavir target the viral capsid to prevent uncoating, while modified versions of the virus are being explored as oncolytic agents for cancer treatment due to their ability to target CD155-expressing tumor cells [10, 11, 17].
Vaccines induce neutralizing antibodies to prevent infection; capsid inhibitors bind to the VP1 pocket to stabilize the virion and prevent RNA release; protease inhibitors block the cleavage of the viral polyprotein; oncolytic therapy utilizes modified virus to directly lyse tumor cells and stimulate an anti-tumor immune response.
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