Poliovirus type 1, 2, 3 (PV1, PV2, PV3)

Poliovirus types 1, 2, and 3 are three distinct serotypes of the enterovirus species *Enterovirus C*, family *Picornaviridae*. These small, non-enveloped RNA viruses are the causative agents of poliomyelitis (“polio”) in humans. Poliovirus is composed of a single-stranded positive-sense RNA genome surrounded by a protein capsid with icosahedral symmetry. Infectivity is initiated by binding to the poliovirus receptor (CD155, or PVR) on the host cell surface, after which the virus enters the cell, releases its RNA genome, and hijacks the host’s protein synthesis machinery for viral replication[3]. Lab and clinical distinction among the three serotypes (PV1, PV2, PV3) is based on differences in the capsid proteins, and all three can cause paralytic disease, though PV1 is most frequently implicated in outbreaks and severe cases[1][3]. Eradication efforts have led to the elimination of wild PV2 and PV3, but circulating vaccine-derived and wild-type PV1 still cause infections in some areas. The primary method of prevention is vaccination, using either inactivated (IPV) or live-attenuated oral (OPV) vaccines[1][3][2].

Other names

Poliovirus serotype 1, Poliovirus serotype 2, Poliovirus serotype 3Poliovirus 1, Poliovirus 2, Poliovirus 3PV-1, PV-2, PV-3Human poliovirus type 1/2/3Brunhilde, Mahoney (type 1 prototype strains)Lansing, MEF-1 (type 2 prototype strains)Leon, Saukett (type 3 prototype strains)

Vaccines induce neutralizing antibodies against viral capsid proteins (predominantly VP1–4). Experimental antivirals block viral uncoating or replication enzymes (RNA-dependent RNA polymerase, proteases), but this is not established therapy.