In the early 20th century, the world was plunged into a state of frenzy. Poliomyelitis, or polio for short, was a formerly sporadic disease caused by poliovirus that had grown to become a global pandemic. At its height, 22000 people in the US alone were left paralysed each year, their motor neurons destroyed (Trevelyan, Smallman-Raynor and Cliff, 2005; Harris and Coyne, in press). By the early 1950s, the “wrath of God”, as the disease had come to be known, was creating widespread panic. Understandably, both the public and health authorities collectively let out a sigh of relief when Jonas Salk discovered the first polio vaccine in 1953.

Despite having been tested initially on only 161 human subjects, Salk’s vaccine, which he called Inactivated Poliovirus Vaccine (IPV) quickly became available on the market (Salk, et al., 1953). Salk’s protocol for producing IPV involved incubating poliovirus in formaldehyde, effectively killing the virus while leaving the viral coat proteins intact. When injected into patients during vaccination, the polio proteins triggered antibody production against the viral proteins (Khan, 2009). Since IPV involved dead pathogens, antibodies were not continually produced and IPV therefore needed to be frequently administered to confer long-term immunity (Khan, 2009). In spite of this downfall, within a year of IPV’s introduction, polio cases in the US dropped from nearly 58000 to just 5600 (Mehndiratta, Mehndiratta and Pande, 2014). Yet victory was to be short-lived. Shortly after laboratories in the US began production of IPV, it was discovered that the batch of vaccine produced by Cutter Laboratories actually resulted in 40000 new cases of polio. Investigations revealed that during IPV production, small populations of the virus had evaded inactivation, and had actually been administered as live virus to patients (Fitzpatrick, 2006). This horrific event came to be known as the Cutter Incident.

Public opinion of IPV quickly declined after the Cutter Incident, leading to the development of an Oral Poliovirus Vaccine (OPV) by Albert Sabin in 1961. Instead of killing the virus, Sabin’s vaccine involved weakening or attenuating the virus by growing it in a foreign host such as monkey kidney epithelial cells (Khan, 2009). This caused adaptations favourable to its survival in the foreign host, but unfavourable to its survival in humans. When injected into a human patient as OPV, the virus grew slowly because it was not adapted to the normal host. OPV was successful in that it mimicked a natural infection and thus triggered both T-cell and antibody responses, requiring only one administration of the vaccine (Khan, 2009). However, health authorities quickly realized that the weakened virus could revert back to its original virulent form, infecting previously vaccinated patients and spreading to other individuals via the fecal-oral route (Modlin and Wenger, 2014). It was realized that OPV therefore was not as effective as previously thought, especially in developing countries with poor hygiene where polio was rampant.

Perhaps because of the downfalls associated with each vaccine, the ensuing decades saw both IPV and OPV undergo tremendous modifications to improve vaccine potency. Today, thanks to Salk and Sabin, combinations of IPV and OPV are used to vaccinate newborns and polio no longer poses a serious health threat to mankind (Faden, 2014). In the span of half a century, vaccines have pushed the polio pandemic to the brink of eradication. Despite this success story, anti-vaccine movements live on. One can only hope that as the public becomes more aware of the power of vaccines, vaccine compliance will improve so that history will not repeat itself.

 

Works Cited

Faden, H., 2014. Poliovirus vaccination : a trilogy. The Journal of Infectious Diseases, 168(1), pp.25–28.

Fitzpatrick, M., 2006. Commentary on “The cutter incident: how America’s first polio vaccine led to a growing vaccine crisis”. Journal of the Royal Society of Medicine, 99, p.156.

Harris, K.G. and Coyne, C.B., in press. Death waits for no man – does it wait for a virus? How enteroviruses induce and control cell death. Cytokine & growth factor reviews.

Khan, F.H., 2009. The elements of immunology. New Delhi: Pearson Education.

Mehndiratta, M.M., Mehndiratta, P. and Pande, R., 2014. Poliomyelitis: historical facts, epidemiology, and current challenges in eradication. The Neurohospitalist, 4(4), pp.223–9.

Modlin, J. and Wenger, J., 2014. Achieving and maintaining polio eradication – new strategies. The New England journal of medicine, 371(16), pp.1476–9.

Salk, J.E., Bennett, B.L., Lewis, L.J., Ward, E.N. and Younger, J.S., 1953. Studies in human subjects on active immunization against poliomyelitis. JAMA, 151(13), pp.1081–98.

Trevelyan, B., Smallman-Raynor, M. and Cliff, A.D., 2005. The spatial dynamics of poliomyelitis in the United States: from epidemic emergence to vaccine-induced retreat, 1910–1971. Annals of the Association of American Geographers, 95(2), pp.269–293.