RT Journal Article
SR Electronic
T1 How polio vaccination affects poliovirus transmission
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 084012
DO 10.1101/084012
A1 Michael Famulare
A1 Guillaume Chabot-Couture
A1 Philip A. Eckhoff
A1 Hil Lyons
A1 Kevin A. McCarthy
A1 Christian Selinger
YR 2016
UL http://biorxiv.org/content/early/2016/10/27/084012.abstract
AB A fundamental complexity of polio eradication is that the elimination of wild poliovirus (WPV) alters the risk-benefit profile of using oral polio vaccine (OPV)—as WPV is eliminated, OPV produces an increasing proportion of the paralytic disease burden since, in rare instances, OPV causes paralysis in vaccine recipients and generates circulating vaccine-derived polio outbreaks (cVDPV) in under-immunized populations. Therefore, to secure the success and long-term stability of polio eradication after the elimination of WPV, OPV use should eventually cease. Type 2 OPV (OPV2) was withdrawn from routine immunization (RI) in April 2016, but detection of type 2 cVDPV has necessitated the use of OPV2 in outbreak response. Thus the world today: RI with OPV2 has stopped, but OPV2 is needed to interrupt outbreaks, and any future OPV2 use several years hence will take place in a population with an unprecedented lack of type 2 immunity. To better understand the complex risk landscape of OPV cessation, we reproducibly summarized data spanning 75 years of polio literature detailing how vaccination affects individual-level susceptibility to infection and viral shedding. We then examined individual-level immunity in the context of close-contact transmission data from the USA and India to quantify the impacts of vaccination on transmission. Our results demonstrate that in settings with inadequate sanitation: (1) OPV has been effective in all populations because it blocks transmission locally, (2) cross-immunity against type 2 produced by bivalent OPV is insufficient to block OPV2 transmission, (3) IPV boosting after prior OPV or WPV exposure is effective for interrupting transmission in settings where inadequate or waning immunity permits significant re-infection, and (4) OPV transmission is limited more by population immunity than attenuation and so the risk of seeding new cVDPV with OPV use will increase substantially a few years after OPV cessation. We conclude with discussion of the implications for policy decisions about IPV and OPV use and vaccine research.Author Summary Oral polio vaccine (OPV) has played an essential role in the elimination of wild poliovirus (WPV), which persists in only three countries. OPV contains live, transmissible viruses that can spread from person-to-person, limited by immunity in OPV recipients and their contacts, and community structure. If OPV spread is insufficiently limited, circulating vaccine-derived poliovirus (cVDPV) outbreaks can occur. After OPV is no longer used in routine immunization, as with the cessation of type 2 OPV this year, population immunity limiting transmission will decline. A key question is how this affects the potential of OPV to spread across communities. To address this, we calculated the relative strengths and roles of immunity, sanitation, and community structure in limiting OPV spread. Our results derive from a detailed review and synthesis of decades of vaccine trial data and community epidemiological studies. Shedding, dose response, and community structure are quantitatively analyzed to systematically explain and model observations of WPV and OPV circulation in low, moderate, and high-transmission settings. We show that within three years of OPV cessation, renewed OPV use will result in propagating OPV transmission and cVDPVs in high-transmission settings, and that this conclusion is compatible with the observed absence of cVDPVs in low-transmission settings.