Poliovirus 3 is the third serotype of poliovirus, a non‑enveloped positive-sense RNA virus in the Picornaviridae family that causes poliomyelitis. It spreads mainly through the fecal‑oral route and infects only humans.
Structure, transmission and epidemiology
Poliovirus 3 is another member of the species Enterovirus C. Its virion has an icosahedral capsid around 30 nm in diameter containing a single-stranded RNA genome of about 7.5 kb. The genome encodes a polyprotein cleaved into structural proteins (VP1–VP4) and non‑structural proteins required for replication. Following ingestion, virus replicates in the pharyngeal and intestinal mucosa and is shed in stool. Transmission occurs via contaminated food, water or hands and, to a lesser extent, respiratory secretions. Humans are the only host. Viremia seeds peripheral tissues; rarely, virus penetrates the central nervous system to damage motor neurons. Three wild poliovirus serotypes circulated before the eradication era. Wild poliovirus type 3 (WPV3) caused fewer outbreaks than type 1. The last reported WPV3 case was in Nigeria in 2012, and WPV3 was declared eradicated worldwide in 2019. Oral polio vaccines containing the Sabin type 3 strain remain part of bivalent formulations, but vaccine‑derived type 3 outbreaks are rare.
Clinical features and notable outbreaks
Most poliovirus 3 infections are asymptomatic or cause mild febrile illness with sore throat and gastrointestinal upset. A small proportion of infections progresses to aseptic meningitis or paralytic poliomyelitis when the virus infects anterior horn motor neurons. Compared with type 1, type 3 is less neurovirulent, and paralysis occurs in roughly 1 in 1000 infections. Before eradication, WPV3 circulated endemically in parts of Asia and Africa and caused outbreaks such as the 2012 cluster in Nigeria. Inadequate vaccination can allow Sabin type 3 vaccine strains to revert to neurovirulence and cause circulating vaccine‑derived poliovirus type 3 (cVDPV3) outbreaks, although these are rare. The removal of the type 2 component from oral vaccines in 2016 shifted focus to bivalent vaccines containing types 1 and 3. High vaccination coverage, environmental surveillance and rapid response teams are essential to prevent re‑emergence of PV3. Poliovirus 3 wild strains have been eradicated, but continued vaccination and surveillance are vital to prevent cVDPV3 outbreaks and sustain a polio‑free world. Maintaining immunity through routine immunisation and supplementary campaigns protects populations from this neurotropic virus. Related Terms: Poliovirus 1, Poliovirus 2, Enterovirus C, Sabin vaccine, Acute flaccid paralysis