The Clinical Times
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Infectious Disease · 1960

Sabin Oral Live-Attenuated Polio Vaccine

Oral Poliovirus Vaccine (OPV)

Portrait of Albert Sabin, developer of the oral polio vaccine
Original uploader was Bobak at the English Wikipedia / Public domain (Wikimedia Commons)

Jonas Salk's killed-virus injectable vaccine, licensed in 1955, halted the worst of the annual American polio epidemics but left an immunological problem unresolved. The inactivated vaccine induced circulating antibody that prevented paralytic disease, but it did not produce robust mucosal immunity in the gastrointestinal tract, which is where wild poliovirus replicates and from which it spreads person to person through fecal-oral transmission. Albert Sabin, a virologist at the University of Cincinnati, had been developing an alternative since the late 1940s: a live vaccine using poliovirus strains attenuated by serial passage through non-human cell cultures until they replicated efficiently in the gut but no longer caused paralysis.

The political and scientific rivalry between Salk and Sabin was sharp, and the U.S. Public Health Service was not prepared to authorize a second large field trial so soon after the 1954 Salk trial. Sabin therefore arranged his definitive mass trials in the Soviet Union, where the polio burden was severe and the public health infrastructure capable of organizing a coordinated national effort. Beginning in 1957 and accelerating through 1959 and 1960, Soviet scientists led by Mikhail Chumakov and Anatoly Smorodintsev administered Sabin's trivalent oral vaccine to more than 10 million children. The results were compelling: attack rates in vaccinated cohorts fell dramatically, and the logistics were far simpler than the Salk regimen.

The United States licensed OPV in 1961. The practical advantages over the injectable vaccine were considerable. No needle was required, so campaigns could be run without medical personnel for each administration. A sugar cube or a few drops on the tongue sufficed. Vaccinated children shed attenuated virus into their communities, extending indirect protection to unvaccinated contacts, a form of herd effect that the inactivated vaccine did not provide. The cost was a fraction of the Salk preparation, which made OPV the practical default for low-income countries.

The WHO launched its Global Polio Eradication Initiative in 1988 using OPV as the primary tool, deploying it in National Immunization Days that reached hundreds of millions of children annually in endemic regions. The strategy succeeded in eliminating wild poliovirus from most of the world: type 2 was certified eradicated in 2015, type 3 in 2019. Wild type 1 persists in a small number of countries, primarily Pakistan and Afghanistan.

The vaccine created its own clinical problem. In populations with low routine immunization coverage, the attenuated strains in OPV can undergo genetic reversion during prolonged gut replication, eventually recovering neurovirulence and causing vaccine-derived poliovirus outbreaks. This risk led the WHO to phase out the type 2 component of OPV in 2016 after wild type 2 eradication, and the strategy has shifted toward inactivated vaccine for routine immunization in higher-income settings. The tension between OPV's exceptional field performance and its small but real neurovirulence risk defines the final phase of the eradication effort Sabin's work made possible.

Key People

Read the original — PubMed

JAMA. 1960;173:1521-1526

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