Poliovirus 2 is the second 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 2 belongs to the species Enterovirus C. Like other polioviruses, it has an icosahedral capsid about 30 nm in diameter that encloses a single-stranded RNA genome. The genome encodes a polyprotein that is cleaved into four structural proteins (VP1–VP4) and non‑structural proteins needed for replication. Following ingestion, virus replicates in the tonsils, oropharyngeal mucosa and intestinal mucosa. Virions are shed in stool and can survive in water for weeks. Infection is usually acquired via contaminated water, food or hands, and less frequently by inhalation of droplets. Only humans are susceptible. Viremia seeds the lymphatics and, in a small fraction of infections, poliovirus crosses the blood‑brain barrier to invade motor neurons of the spinal cord and brainstem, leading to flaccid paralysis. Three wild poliovirus serotypes circulated historically. Wild poliovirus type 2 (WPV2) was last detected in northern India in 1999 and was declared eradicated. However, mutated Sabin type 2 strains in oral polio vaccine can regain neurovirulence and cause circulating vaccine‑derived poliovirus type 2 (cVDPV2) outbreaks in areas with poor immunisation.
Clinical significance and public health issues
Infection with poliovirus 2 is asymptomatic in about 90 % of cases. When illness occurs, patients typically experience low‑grade fever, sore throat and gastrointestinal upset. A transient viremia sometimes seeds the meninges and causes aseptic meningitis. In rare cases, invasion of anterior horn motor neurons leads to acute flaccid paralysis affecting the limbs, respiratory muscles or cranial nerves. Survivors may develop muscle weakness or post‑polio syndrome decades later. The global switch from trivalent to bivalent oral polio vaccine in 2016 removed the type 2 component to reduce the risk of cVDPV2. Nonetheless, outbreaks of vaccine‑derived poliovirus type 2 have occurred in Nigeria, Democratic Republic of Congo and the Philippines, underscoring the need for high vaccination coverage and rapid outbreak response. Containment of PV2 in laboratories and vaccine production facilities is now mandated to prevent accidental release. Poliovirus 2 wild strains have been eradicated, but vaccine‑derived type 2 strains continue to pose a risk in under‑immunised communities. Sustaining high levels of routine immunisation and strict containment of PV2 materials are essential to prevent re‑establishment of poliovirus transmission. Control efforts rely on surveillance for acute flaccid paralysis and prompt response to any detected cVDPV2. Related Terms: Poliovirus 1, Poliovirus 3, Enterovirus C, Sabin vaccine, Coxsackievirus