Abstract
Background.Comparing model expectations with the experience of oral poliovirus vaccine (OPV) containing serotype 2 (OPV2) cessation can inform risk management for the expected cessation of OPV containing serotypes 1 and 3 (OPV13). Methods.We compare the expected post-OPV2-cessation OPV2-related viruses from models with the evidence available approximately 6 months after OPV2 cessation. We also model the trade-offs of use vs nonuse of monovalent OPV (mOPV) for outbreak response considering all 3 serotypes.Results.Although too early to tell definitively, the observed die-out of OPV2-related viruses in populations that attained sufficiently intense trivalent OPV (tOPV) use prior to OPV2 cessation appears consistent with model expectations. As expected, populations that did not intensify tOPV use prior to OPV2 cessation show continued circulation of serotype 2 vaccine-derived polioviruses (VDPVs). Failure to aggressively use mOPV to respond to circulating VDPVs results in a high risk of uncontrolled outbreaks that would require restarting OPV.Conclusions.Ensuring a successful endgame requires more aggressive OPV cessation risk management than has occurred to date for OPV2 cessation. This includes maintaining high population immunity to transmission up until OPV13 cessation, meeting all prerequisites for OPV cessation, and ensuring sufficient vaccine supply to prevent and respond to outbreaks.
Highlights
Comparing model expectations with the experience of oral poliovirus vaccine (OPV) containing serotype 2 (OPV2) cessation can inform risk management for the expected cessation of OPV containing serotypes 1 and 3 (OPV13)
Too early to tell definitively, the observed die-out of OPV2-related viruses in populations that attained sufficiently intense trivalent OPV use prior to OPV2 cessation appears consistent with model expectations
Failure to aggressively use monovalent OPV (mOPV) to respond to circulating vaccine-derived poliovirus (VDPV) results in a high risk of uncontrolled outbreaks that would require restarting OPV
Summary
We compare the expected post-OPV2-cessation OPV2-related viruses from models with the evidence available approximately 6 months after OPV2 cessation. We reviewed the evidence available approximately 6 months after OPV2 cessation and compared the experience far with precessation risk model expectations. For WPV and any stage of OPV-related virus, the DEB model simplifies the stochastic and local process of die-out by assuming that no new transmissions can occur once the infectiousness-weighted prevalence drops below a threshold of 5 per million people (ie, the transmission threshold), based on calibration of the model to evidence with WPV die-out and persistence and cVDPV emergence in a diverse set of populations [7]. Our analysis of die-out reports the proportion of all 610 OPVusing subpopulations that still experience OPV2-related virus transmission as a function of time after OPV2 cessation (ie, the proportion in which the prevalence remains above the transmission threshold for at least 1 of the OPV2 reversion stages)
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