The polioviruses (PVs) are mainly transmitted by direct contact with an infected person through the fecal-oral route and respiratory secretions (or more rarely via contaminated water or food) and have a primary tropism for the gut. After their replication in the gut, in rare cases (far less than 1% of the infected individuals), PVs can spread to the central nervous system leading to flaccid paralysis, which can result in respiratory paralysis and death. By the middle of the 20th century, every year the wild polioviruses (WPVs) are supposed to have killed or paralyzed over half a million people. The introduction of the oral poliovirus vaccines (OPVs) through mass vaccination campaigns (combined with better application of hygiene measures), was a success story which enabled the World Health Organization (WHO) to set the global eradication of poliomyelitis as an objective. However this strategy of viral eradication has its limits as the majority of poliomyelitis cases today arise in individuals infected with circulating vaccine-derived polioviruses (cVDPVs) which regain pathogenicity following reversion or recombination. In recent years (between January 2018 and May 2023), the WHO recorded 8.8 times more cases of polio which were linked to the attenuated OPV vaccines (3,442 polio cases after reversion or recombination events) than cases linked to a WPV (390 cases). Recent knowledge of the evolution of RNA viruses and the exchange of genetic material among biological entities of the intestinal microbiota, call for a reassessment of the polio eradication vaccine strategies.
Although there have been no cases of serotype 2 wild poliovirus for more than 20 years, vaccine continued for years with the oral poliovirus vaccine (OPV2) as part of trivalent vaccine (tOPV, containing serotype 1, 2, and 3). However, OPV2 was reported to generate paralytic serotype 2 vaccine-derived poliovirus (cVDPV2) outbreaks in several continents even after withdrawal of OPV2 in April 2016 (1). It represents an obstacle to achieving polio eradication and populations with low immunization coverage are particularly at risk of cVDPV2 spread (as well as cVDPV1 and cVDPV3).