Abstract
The oral polio vaccine (OPV) contains live-attenuated polioviruses that induce immunity by causing low virulence infections in vaccine recipients and their close contacts. Widespread immunization with OPV has reduced the annual global burden of paralytic poliomyelitis by a factor of 10,000 or more and has driven wild poliovirus (WPV) to the brink of eradication. However, in instances that have so far been rare, OPV can paralyze vaccine recipients and generate vaccine-derived polio outbreaks. To complete polio eradication, OPV use should eventually cease, but doing so will leave a growing population fully susceptible to infection. If poliovirus is reintroduced after OPV cessation, under what conditions will OPV vaccination be required to interrupt transmission? Can conditions exist in which OPV and WPV reintroduction present similar risks of transmission? To answer these questions, we built a multi-scale mathematical model of infection and transmission calibrated to data from clinical trials and field epidemiology studies. At the within-host level, the model describes the effects of vaccination and waning immunity on shedding and oral susceptibility to infection. At the between-host level, the model emulates the interaction of shedding and oral susceptibility with sanitation and person-to-person contact patterns to determine the transmission rate in communities. Our results show that inactivated polio vaccine (IPV) is sufficient to prevent outbreaks in low transmission rate settings and that OPV can be reintroduced and withdrawn as needed in moderate transmission rate settings. However, in high transmission rate settings, the conditions that support vaccine-derived outbreaks have only been rare because population immunity has been high. Absent population immunity, the Sabin strains from OPV will be nearly as capable of causing outbreaks as WPV. If post-cessation outbreak responses are followed by new vaccine-derived outbreaks, strategies to restore population immunity will be required to ensure the stability of polio eradication.
Highlights
Wild polioviruses (WPVs) have been eliminated from all but three countries [1,2] by mass vaccination with the oral polio vaccine (OPV)
In its attenuated form, this spread is beneficial as it generates population immunity
We show that in high transmission rate settings, falling population immunity after OPV cessation will lead to conditions in which OPV and WPV are capable of causing outbreaks, and that this conclusion is compatible with the known safety of OPV prior to global cessation
Summary
Wild polioviruses (WPVs) have been eliminated from all but three countries [1,2] by mass vaccination with the oral polio vaccine (OPV). OPV has been the preferred vaccine for polio eradication because it costs less, can be reliably delivered by volunteers without medical training, and is more effective against poliovirus infection, relative to the inactivated polio vaccine (IPV) [3,4]. Unique among current human vaccines, the live-attenuated Sabin poliovirus strains in OPV are transmissible. This transmissibility provides additional passive immunization that enhances the effectiveness of OPV for generating herd immunity. The attenuation of Sabin OPV is unstable and so it can, in rare instances, cause paralytic poliomyelitis [5] and lead to outbreaks of circulating vaccine-derived poliovirus (cVDPV) with virulence and transmissibility comparable to that of WPV strains [6]. To complete the task of poliovirus eradication, vaccination with Sabin OPV must eventually cease [7]
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