Summary overview of Kid Risk, Inc. research on poliovirus risk management (as of July 2017)

Motivated by an interest in appropriately integrating economic, risk, decision, and dynamic disease models to demonstrate the difference between static and dynamic policy models, our polio modeling efforts began in 2001 when we decided to retrospectively characterize the economic benefits of polio risk management in the United States.(1) Discussions in late 2001 with subject matter experts at the US Centers for Disease Control and Prevention led to our focus on the polio endgame since 2002. We characterized the decision options for post-wild poliovirus (WPV) eradication policies,(2) and developed a differential equation-based dynamic transmission model that included characterization of immunity states associated with WPV infection and vaccination with either oral poliovirus vaccine (OPV) or inactivated poliovirus vaccine (IPV), including asymptomatic infections.(3) Given exclusive use of trivalent OPV (tOPV) at that time, the model characterized a generic serotype and did not consider OPV evolution endogenously.(3) We focused on the global policy level and developed estimates of the costs for the different post WPV-eradication decision options,(4) which we stratified by World Bank Income levels to capture important differences that exist between countries. We also characterized the costs and value of the global poliovirus surveillance system.(5) We provided the first estimates of the risks of vaccine-associated paralytic polio (VAPP) and vaccine-derived polioviruses (VDPVs), including circulating VDPVs (cVDPVs) and immunodeficiency-associated VDPVs (iVDPVs), based on statistical analyses of available data and as a function of different post-WPV eradication policies.(6) We explored post-WPV eradication outbreak response policies, and this analysis provided key insights to the GPEI in 2005 about the benefits of both pre- and post-WPV eradication outbreak response,(7) which led to significant improvements in GPEI outbreak response activities. Most of these papers appeared in a 2006 special issue of Risk Analysis,(8) which also included our perspectives on risk management in a polio-free world (9) and on the collaborative modeling process we created.(10) Our retrospective economic analysis showed significant (hundreds of billions of dollars) net benefits for the US,(1) which helped to strengthen US commitments to polio risk management.

Following the development of all of the model components, we focused on an economic analysis of post-eradication immunization policies. Given the long time horizons considered in the economic analyses, our integrated model included consideration of potential reinfection and asymptomatic participation in transmission of individuals with waned immunity, with paralysis only occurring in fully susceptible individuals. High-level policy discussions related to control vs. eradication in late 2006 motivated us to use our model to estimate the economics of eradication (followed by several different post-WPV eradication immunization policies) compared to a wide range of control options, which demonstrated that eradication represented a better health and economic option than control.(11) Some discussions at the time included significant pessimism about the ability to stop poliovirus transmission in India, and we used our model to suggest that elimination could occur in India with sufficient immunization intensity.(11) We also demonstrated the economic inefficiency of a wavering global commitment to eradication.(11) The economic analysis of post-WPV eradication immunization policies showed that either stopping OPV altogether or switching to IPV dominated continued OPV use after successful eradication of WPVs.(12) IPV represented the option with the highest expected costs but lowest expected cases, while stopping poliovirus immunization represented an option with lower expected costs but some additional expected cases, which led us to recommend research and investment into strategies to reduce IPV costs.(12) We performed extensive uncertainty and sensitivity analyses.(13) These analyses led to recognition of the need for global coordination of OPV cessation and creation of a stockpile for post-WPV eradication outbreak response,(14) and recognition of the importance of ensuring sufficient resources for polio eradication to succeed.(15) Building on our prior analysis of a wavering commitment,(11) we explored the dynamics of priority shifting for eradicable diseases.(16) Recognizing the importance of a stockpile of OPV for post-WPV eradication outbreak response,(14) we developed a framework for optimal stockpile design.(17) We developed an individual-based model version of our polio dynamic disease transmission model that showed the significance of different assumptions about mixing networks.(18) We performed an economic analysis that estimated 40-50 billion US dollars in net benefits for the Global Polio Eradication Initiative (GPEI) for which our range of estimates depended on whether successfully-coordinated OPV cessation following WPV eradication included global use of IPV or not.(19) We contributed to discussions about the role of economic analyses in evaluation global disease management efforts (20) and the development of eradication investment cases.(21) In 2012, we explored trends in the risks of poliovirus transmission in the US, and we recognized that imported live polioviruses (LPVs) could potentially circulate in a population with high IPV coverage, although the risks in the US appeared low.(22) We also explored the probability of undetected wild poliovirus circulation after apparent global interruption of transmission by extending a simple conceptual analysis.(23)

As the GPEI immunization policies evolved, including widespread use of bivalent OPV (bOPV) for supplemental immunization activities (SIAs), we appreciated the need to expand and update our integrated model. Recognizing the important role of modeling population immunity,(24) and its key role in prevention (25) and we characterized the current global immunization policy options and prerequisites for OPV cessation.(26) We developed a series of papers published in a 2013 special issue of Risk Analysis describing the components of our expanded and updated poliovirus transmission and OPV evolution model.(27) We performed a comprehensive expert review of the literature on poliovirus immunity and transmission,(28) and synthesized the information from the experts to (i) numerically characterize an expanded set of immunity states for the model and (ii) identify significant uncertainties despite the large literature.(29) We reviewed the 2012 national polio immunization strategies to characterize current aggregate global policies, and we reviewed the seroconversion literature to characterize variability in vaccine take rates for different vaccines and numbers of doses in different settings.(30) We also updated our prior review of cVDPV risks(6) and reviewed the literature related to understanding and modeling OPV evolution.(31) This analysis (31) allowed us to include OPV evolution and the creation of cVDPVs endogenously in our expanded poliovirus transmission and OPV evolution model,(32) which led us to conclude that our prior statistical model for cVDPV risks(6) provided reduced predictive value due to the global shift from exclusive tOPV use until WPV eradication to a strategy of phased serotype-specific OPV cessation. We focused on the need to manage population immunity to transmission considering all individuals in the population, including individuals immune to disease but able to contribute asymptomatically to transmission, most notably those with only IPV-induced immunity.(33) Our expanded model of poliovirus transmission and OPV evolution offered insights from modeling a diverse set of actual experiences with wild and vaccine-related polioviruses.(32) Overall, the expanded poliovirus transmission and OPV evolution model: (i) uses 8 recent immunity states to reflect immunity derived from maternal antibodies, only IPV vaccination, only LPV infection, or both IPV vaccination and LPV infection (to more realistically capture the differences in immunity derived from IPV and LPV), (ii) includes multi-stage waning and infection processes (for more realistic characterization of these processes), (iii) characterizes OPV evolution as a 20-stage process from OPV as administered to fully-reverted polioviruses with assumed identical properties to typical homotypic WPVs (to allow cVDPV emergence to occur within the model), (iv) characterizes each serotype separately (to analyze serotype-specific vaccination policies and risks), (v) considers explicitly both fecal-oral and oropharyngeal transmission (to account for the differential impact of IPV on fecal and oropharyngeal excretion), (vi) accounts for heterogeneous preferential mixing between mixing age groups and subpopulations, and (vii) accounts for differences between various IPV and OPV routine immunization schedules and the reality of repeatedly missed children during successive SIAs.(32,34,35)

In 2014, we updated our estimates of IPV costs in the context of exploring national choices related to IPV use with various delivery options.(36) We also modeled the dynamics of OPV cessation without (37) and with IPV,(38) which demonstrated the importance of using sufficient amounts of tOPV in the run up to OPV cessation and the relatively small role that IPV might play in areas with conditions conducive to poliovirus transmission (i.e., relatively high R0, high contribution of fecal-oral transmission). We used our transmission model (32) to characterize the potential impact of expanding target age groups for polio SIAs,(34) and to stop and prevent poliovirus transmission in two high-risk areas in northern India (35) and in the high-risk area of northwest Nigeria.(39) We used an individual-based model to characterize the potential for transmission of polioviruses following introduction into Amish communities in North America.(40) Consistent with our prior recognition of potential circulation of LPVs in areas with high IPV coverage,(22) following the observation of WPV serotype 1 transmission in Israel, we modeled population immunity to transmission and management strategies for Israel.(41) Insights from our modeling suggest the importance of focusing on immunization program performance to maintain population immunity to transmission, as the key to success in the polio endgame.(42) Many of our recent modeling studies emphasize the failure to vaccinate as the primary cause of delay in achieving and maintaining WPV eradication, and the importance of heterogeneity in populations that leads to pockets of preferentially-mixing under-immunized individuals that can sustain transmission.(34,35,39-41) In contrast to some other areas in the US, we recently reported relatively little heterogeneity in six counties in Central Florida at high risk of importations due to international family attractions.(43) We presented and published highlights of the policy impacts of our modeling for which we received the 2014 INFORMS Edelman Award.(44)

In 2015, we provided an overview of the information from different types of poliovirus surveillance activities and we modeled the potential for undetected live poliovirus circulation after apparent interruption of transmission,(45) based on our earlier exploration (23) of a theoretical analysis that quantified undetected circulation in a hypothetical population. We characterized global importations and cVDPVs since 2000 and showed that over 50 countries failed to maintain sufficient population immunity to transmission to prevent paralytic cases from cVDPVs or imported WPVs.(46) We also modeled three countries that use IPV-only for routine immunization (the US, the Netherlands, and Israel) and demonstrated the decline in population immunity in transmission that occurs when countries switch from using OPV to using IPV-only.(46) An editorial related to an article that reviewed the safety data for IPV in the US described the good news for billions of children who will receive IPV with the global introduction of IPV in all OPV-using countries.(47) Looking closely at northwest Nigeria, we explored the trade-offs associated with different strategies to manage population immunity to transmission that demonstrated the importance of using more tOPV in SIAs in the run-up to OPV2 cessation.(48)

We published a series of articles in a special issue of BMC Infectious Diseases on integrated modeling and management of poliovirus endgame risks and policies that aimed to help national, regional, and global health leaders as they navigate the polio endgame from 2013-2052. Modeling the long-term risks requires characterization of the potential for reintroductions of iVDPVs from a small number of individuals with primary B-cell-related immune-deficiencies,(49) for which we reviewed the evidence collected since our 2006 analysis.(6) We developed and used an integrated global model that characterized the risks, costs, and benefits of different future poliovirus risk management options for 2013-2052 compared to the 2013 baseline that included continued widespread use of OPV.(50) Using both the global model (50) and a model of northern Nigeria,(48) we showed the importance of vaccine choice and preferential use of tOPV in the run up to globally-coordinated cessation of serotype 2 OPV (i.e., OPV2 cessation) then-planned and since implemented in late April 2016.(51) Recognizing the importance of significant tOPV use, we estimated tOPV and bOPV needs through 2020.(52) As global health policy makers were approaching the final decision point for establishing the timing of OPV2 cessation, we explored alternative OPV cessation timing options.(53) We demonstrated the importance of rapid and aggressive outbreak response after OPV cessation and during the polio endgame.(54) In anticipation of coordinated OPV2 cessation, we explored the risks of potential non-synchronous OPV2 cessation (55) and of inadvertent tOPV use after OPV2 cessation.(56)

For the global model (50) we performed an uncertainty and sensitivity analysis of cost assumptions.(57) Recognizing the importance of maintaining high population immunity for serotypes 1 and 3 prior to future coordinated bOPV cessation, we demonstrated the benefits of high levels of continued bOPV use and sustaining OPV production through bOPV cessation.(58) Building on our prior characterization of iVDPV risks,(49) we modeled the impact of comprehensive screening to find and treat asymptomatic iVDPV excretors.(59) We explored the potential benefits of investments in a new poliovirus vaccine assuming the best attributes of OPV and IPV.(60) We highlighted the importance of maintaining preparedness throughout the polio endgame.(61) We demonstrated the minor role of IPV in outbreak response when used in conjunction with OPV and showed that IPV in addition to OPV for outbreak response does not represent a cost-effective option compared to using OPV alone.(62) We also explored the need to maintain suffiicient poliovirus vaccine supplies and stockpiles for outbreak response in the polio endgame.(63) We assessed the economic benefits of temporary recommendations for international travel immunization requirements for countries with transmission of serotype 1 wild polioviruses(64) Recognizing the increasing role of environmental surveillance for polioviruses, we systematically reviewed published poliovirus environmental surveillance studies and reported information related to the design, cost, and effectiveness of these systems.(65) We also explored the dynamics of die-out of serotype 2 polioviruses after homotypic OPV cessation and lessons learned from its cessation relevant to the cessation of serotypes 1 and 3.(66) Reviewing insights from prior modeling,(34,35,39-41) we demonstrated how under-vaccinated subpopulations can sustain poliovirus transmission despite high coverage in the surrounding population, depending on the degree of mixing and the size of the under-vaccinated subpopulation.(67)

References

1. Thompson KM, Duintjer Tebbens RJ. Retrospective cost-effectiveness analyses for polio vaccination in the United States. Risk Anal 2006;26(6):1423-1440.
2. Sangrujee N, Duintjer Tebbens RJ, Cáceres VM, Thompson KM. Policy decision options during the first 5 years following certification of polio eradication. Medscape Gen Med 2003;5(4):35.
3. Duintjer Tebbens RJ, Pallansch MA, Kew OM, Cáceres VM, Sutter RW, Thompson KM. A dynamic model of poliomyelitis outbreaks: Learning from the past to help inform the future. Am J Epidemiol 2005;162(4):358-372.
4. Duintjer Tebbens RJ, Sangrujee N, Thompson KM. The costs of polio risk management policies after eradication. Risk Anal 2006;26(6):1507-1531.
5. de Gourville EM, Sangrujee N, Duintjer Tebbens RJ, Pallansch MA, Thompson KM. Global surveillance and the value of information: The case of the global polio laboratory network. Risk Anal 2006;26(6):1557-1569.
6. Duintjer Tebbens RJ, Pallansch MA, Kew OM, Cáceres VM, Jafari H, Cochi SL, Aylward RB, Thompson KM. Risks of paralytic disease due to wild or vaccine-derived poliovirus after eradication. Risk Anal 2006;26(6):1471-1505.
7. Thompson KM, Duintjer Tebbens RJ, Pallansch MA. Evaluation of response scenarios to potential polio outbreaks using mathematical models. Risk Anal 2006;26(6):1541-1556.
8. Thompson KM. Poliomyelitis and the role of risk analysis in global infectious disease policy and management. Risk Anal 2006;26(6):1419-1421.
9. Aylward RB, Sutter RW, Cochi SL, Thompson KM, Jafari H, Heymann DL. Risk management in a polio-free world. Risk Anal 2006;26(6):1441-1448.
10. Thompson KM, Duintjer Tebbens RJ, Pallansch MA, Kew OM, Sutter RW, Aylward RB, Watkins M, Gary HE, Jr., Alexander JP, Jr., Venczel L, Johnson D, Cáceres VM, Sangrujee N, Jafari H, Cochi SL. Development and consideration of global policies for managing the future risks of poliovirus outbreaks: Insights and lessons learned through modeling. Risk Anal 2006;26(6):1571-1580.
11. Thompson KM, Duintjer Tebbens RJ. Eradication versus control for poliomyelitis: An economic analysis. Lancet 2007;369(9570):1363-1371.
12. Thompson KM, Duintjer Tebbens RJ, Pallansch MA, Kew OM, Sutter RW, Aylward RB, Watkins M, Gary HE, Jr., Alexander JP, Jr., Jafari H, Cochi SL. The risks, costs, and benefits of possible future global policies for managing polioviruses. Am J Public Health 2008;98(7):1322-1330.
13. Duintjer Tebbens RJ, Pallansch MA, Kew OM, Sutter RW, Aylward RB, Watkins M, Gary HE, Jr., Alexander JP, Jr., Jafari H, Cochi SL, Thompson KM. Uncertainty and sensitivity analyses of a decision analytic model for post-eradication polio risk management. Risk Anal 2008;28(4):855-876.
14. Thompson KM, Duintjer Tebbens RJ. The case for cooperation in managing and maintaining the end of poliomyelitis: Stockpile needs and coordinated OPV cessation. Medscape J Med 2008;10(8):190.
15. Thompson KM, Duintjer Tebbens RJ. Using system dynamics to develop policies that matter: Global management of poliomyelitis and beyond. Syst Dynam Rev 2008;24(4):433-449.
16. Duintjer Tebbens RJ, Thompson KM. Priority shifting and the dynamics of managing eradicable infectious disease. Manage Sci 2009;55(4):650-663.
17. Duintjer Tebbens RJ, Pallansch MA, Alexander JP, Jr., Thompson KM. Optimal vaccine stockpile design for an eradicated disease: Application to polio. Vaccine 2010;28(26):4312-4327.
18. Rahmandad H, Hu K, Duintjer Tebbens RJ, Thompson KM. Development of an individual-based model for polioviruses: Implications of the selection of network type and outcome metrics. Epidemiol & Infect 2010;139(6):836-848.
19. Duintjer Tebbens RJ, Pallansch MA, Cochi SL, Wassilak SGF, Linkins J, Sutter RW, Aylward RB, Thompson KM. Economic analysis of the Global Polio Eradication Initiative. Vaccine 2011;29(2):334-343.
20. Thompson KM, Duintjer Tebbens RJ. Challenges related to the economic evaluation of the direct and indirect benefits and the costs of disease elimination and eradication efforts. Disease Eradication in the 21st Century: Implications for Global Health. Cambridge, MA: MIT Press: 2011; 115-130.
21. Thompson KM, Rabinovich R, Conteh L, Emerson CI, Hall BF, Singer PA, Vijayaraghavan M, Walker DG. Developing an eradication investment case. Disease Eradication in the 21st Century: Implications for Global Health. Cambridge, MA: MIT Press: 2011; 133-148.
22. Thompson KM, Wallace GS, Duintjer Tebbens RJ, Smith PH, Barskey AE, Pallansch MA, Gallagher KM, Alexander JP, Armstrong GL, Cochi SL, Wassilak SG. Trends in the risk of U.S. Polio outbreaks and poliovirus vaccine availability for response. Public Health Rep 2012;127(1):23-37.
23. Kalkowska DA, Duintjer Tebbens RJ, Thompson KM. The probability of undetected wild poliovirus circulation after apparent global interruption of transmission. Am J Epidemiol 2012;175(9):936-949.
24. Thompson KM. The role of risk analysis in polio eradication: Modeling possibilities, probabilities and outcomes to inform choices. Expert Rev Vaccines 2012;11(1):5-7.
25. Thompson KM. Valuing prevention as the new paradigm in global health: Managing population immunity For vaccine-preventable diseases ICU Management 2012; 12(4):9-11.
26. Thompson KM, Duintjer Tebbens RJ. Current polio global eradication and control policy options: Perspectives from modeling and prerequisites for OPV cessation. Exp Rev Vaccines 2012;11(4):449-459.
27. Thompson KM. Modeling poliovirus risks and the legacy of polio eradication. Risk Anal 2013;33(4):505-515.
28. Duintjer Tebbens RJ, Pallansch MA, Chumakov KM, Halsey NA, Hovi T, Minor PD, Modlin JF, Patriarca PA, Sutter RW, Wright PF, Wassilak SG, Cochi SL, Kim JH, Thompson KM. Expert review on poliovirus immunity and transmission. Risk Anal 2013;33(4):544-605.
29. Duintjer Tebbens RJ, Pallansch MA, Chumakov KM, Halsey NA, Hovi T, Minor PD, Modlin JF, Patriarca PA, Sutter RW, Wright PF, Wassilak SGF, Cochi SL, Kim J-H, Thompson KM. Review and assessment of poliovirus immunity and transmission: Synthesis of knowledge gaps and identification of research needs. Risk Anal 2013;33(4):606-646.
30. Thompson KM, Pallansch MA, Duintjer Tebbens RJ, Wassilak SG, Kim J-H, Cochi SL. Pre-eradication vaccine policy options for poliovirus infection and disease control. Risk Anal 2013;33(4):516-543.
31. Duintjer Tebbens RJ, Pallansch MA, Kim J-H, Burns CC, Kew OM, Oberste MS, Diop O, Wassilak SGF, Cochi SL, Thompson KM. Review: Oral poliovirus vaccine evolution and insights relevant to modeling the risks of circulating vaccine-derived polioviruses (cVDPVs). Risk Anal 2013;23(4):680-702.
32. Duintjer Tebbens RJ, Pallansch MA, Kalkowska DA, Wassilak SG, Cochi SL, Thompson KM. Characterizing poliovirus transmission and evolution: Insights from modeling experiences with wild and vaccine-related polioviruses. Risk Anal 2013;23(4):703-749.
33. Thompson KM, Pallansch MA, Duintjer Tebbens RJ, Wassilak SGF, Cochi SL. Modeling population immunity to support efforts to end the transmission of live polioviruses. Risk Anal 2013;33(4):647-663.
34. Duintjer Tebbens RJ, Kalkowska DA, Wassilak SG, Pallansch MA, Cochi SL, Thompson KM. The potential impact of expanding target age groups for polio immunization campaigns. BMC Infect Dis. 2014;14:45.
35. Kalkowska DA, Duintjer Tebbens RJ, Thompson KM. Modeling strategies to increase population immunity and prevent poliovirus transmission in two high-risk areas in northern India. J Infect Dis 2014;210(S1):398-411.
36. Thompson KM, Duintjer Tebbens RJ. National choices related to inactivated poliovirus vaccine, innovation and the endgame of global polio eradication. Expert Rev Vaccines 2014;13(2):221-34.
37. Thompson KM, Duintjer Tebbens RJ. Modeling the dynamics of oral poliovirus vaccine cessation. J Infect Dis 2014;210(S1):475-484.
38. Duintjer Tebbens RJ, Thompson KM. Modeling the potential role of inactivated poliovirus vaccine to manage the risks of oral poliovirus vaccine cessation. J Infect Dis 2014;210(S1):485-497.
39. Kalkowska DA, Duintjer Tebbens RJ, Thompson KM. Modeling strategies to increase population immunity and prevent poliovirus transmission in the high-risk area of northwest Nigeria. J Infect Dis 2014;210(S1):412-423.
40. Kisjes KH, Duintjer Tebbens RJ, Wallace GS, Pallansch MA, Cochi SL, Wassilak SGF, Thompson KM. Individual-based modeling of potential poliovirus transmission in connected religious communities in North America with low uptake of vaccination. J Infect Dis 2014;210(S1):424-433.
41. Kalkowska DA, Duintjer Tebbens RJ, Grotto I, Shulman LM, Anis E, Wassilak SGF, Pallansch MA, Thompson KM. Modeling options to manage type 1 wild poliovirus imported into Israel in 2013. J Infect Dis 2015;211(11):1800-1812.
42. Thompson KM. Polio endgame management: Focusing on performance with or without inactivated poliovirus vaccine. Lancet 2014;384(9953):1480-2.
43. Thompson KM, Logan GE, Research Team from Florida SHOTS™. Characterization of heterogeneity in childhood immunization coverage in central Florida using immunization registry data. Risk Anal 2015:2 Jun doi: 10.1111/risa.12424.
44. Thompson KM, Duintjer Tebbens RJ, Pallansch MA, Wassilak SGF, Cochi SL. Polio eradicators use analytical models to make better decisions. Interfaces 2015;45(1):5-25.
45. Kalkowska DA, Duintjer Tebbens RJ, Pallansch MA, Cochi SL, Wassilak SGF, Thompson KM. Modeling undetected live poliovirus circulation after apparent interruption of transmission: Implications for surveillance and vaccination. BMC Infect Dis 2015;15:66, doi: 10.1186/s12879-015-0791-5.
46. Thompson KM, Kalkowska DA, Duintjer Tebbens RJ. Managing population immunity to reduce or eliminate the risks of circulation following the importation of polioviruses. Vaccine 2015;33(13):1568-1577.
47. Thompson KM. Good news for billions of children who will receive IPV. Lancet Infect Dis 2015; 15(10):1120–1122, doi: http://dx.doi.org/10.1016/S1473-3099(15)00099-7.
48. Duintjer Tebbens RJ, Pallansch MA, Wassalik SGF, Cochi SL, Thompson KM. Combinations of quality and frequency of immunization activities to stop and prevent poliovirus transmission in the high-risk area of northwest Nigeria. PLoS One 2015;10(6):e0130123, doi: 10.1371/journal.pone.0130123.
49. Duintjer Tebbens RJ, Pallansch MA, Thompson KM. Modeling the prevalence of immunodeficiency-associated long-term vaccine-derived poliovirus excretors and the potential benefits of antiviral drugs. BMC Infect Dis 2015; 15:379, doi: 10.1186/s12879-015-1115-5.
50. Duintjer Tebbens RJ, Pallansch MA, Cochi SL, Wassalik SGF, Thompson KM. An economic analysis of poliovirus risk management policy options for 2013-2052. BMC Infect Dis 2015; 15:389, doi: 10.1186/s12879-015-1112-8.
51. Thompson KM, Duintjer Tebbens RJ. The differential impact of oral poliovirus vaccine formulation choices on serotype-specific population immunity to poliovirus transmission. BMC Infect Dis 2015; 15:376, doi: 10.1186/s12879-015-1116-4.
52. Duintjer Tebbens RJ, Thompson KM. Managing the risk of circulating vaccine-derived poliovirus during the endgame: Oral poliovirus vaccine needs. BMC Infect Dis 2015; 15:390, doi: 10.1186/s12879-015-1114-6.
53. Thompson KM, Duintjer Tebbens RJ. Health and economic consequences of different options for timing the coordinated global cessation of the three oral poliovirus vaccine serotypes. BMC Infect Dis 2015; 15:374, doi: 10.1186/s12879-015-1113-7.
54. Duintjer Tebbens RJ, Pallansch MA, Wassalik SGF, Cochi SL, Thompson KM. Characterization of outbreak response strategies and potential vaccine stockpile needs for the polio endgame. BMC Infect Dis 2016; 16:137, doi: 10.1186/s12879-016-1465-7.
55. Duintjer Tebbens RJ, Hampton LM, Thompson KM. Implementation of coordinated serotype 2 oral poliovirus vaccine cessation: Risks of potential non-synchronous cessation. BMC Infect Dis 2016; 16:231, doi: 10.1186/s12879-016-1536-9.
56. Duintjer Tebbens RJ, Hampton LM, Thompson KM. Implementation of coordinated global serotype 2 oral poliovirus vaccine cessation: Risks of inadvertent trivalent oral poliovirus vaccine use. BMC Infect Dis 2016; 16:237, doi: 10.1186/s12879-016-1537-8.
57. Duintjer Tebbens RJ, Thompson KM. Uncertainty and sensitivity analysis of cost assumptions for global long-term poliovirus risk management. J Vaccines & Vaccination 2016; 7:5; doi: 10.4172/2157-7560.1000339.
58. Duintjer Tebbens RJ, Hampton LM, Wassilak SGF, Pallansch MA, Cochi SL, Thompson KM. Maintenance and intensification of bivalent oral poliovirus vaccine use prior to its coordinated global cessation. J Vaccines & Vaccination 2016; 7:5, doi: 10.4172/2157-7560.1000340.
59. Duintjer Tebbens RJ, Thompson KM. Comprehensive screening for immunodeficiency-associated vaccine-derived poliovirus: An essential OPV cessation risk management strategy. Epidemiol & Infect 2016; doi:10.1017/S0950268816002302.
60. Duintjer Tebbens RJ, Thompson KM. The potential benefits of a new poliovirus vaccine for long-term poliovirus risk management. Future Microbiol 2016; 11:1549-61.
61. Thompson KM, Duintjer Tebbens RJ. How should we prepare for an outbreak of reintroduced live polioviruses? Future Virol 2017; 12(2):41-44, doi: 10.2217/fvl-2016-0131.
62. Duintjer Tebbens RJ, Thompson KM. Costs and benefits of including inactivated in addition to oral poliovirus vaccine in outbreak response after cessation of oral poliovirus vaccine use. Medical Decision Making Policy & Practice 2017; doi: 10.1177/2381468317697002.
63. Duintjer Tebbens RJ, Thompson KM. Poliovirus vaccination during the endgame: Insights from integrated modeling Medical Decision Making Policy & Practice 2017; doi:10.1177/2381468317697002.
64. Duintjer Tebbens RJ, Thompson KM. Modeling the costs and benefits of temporary recommendations for poliovirus exporting countries to Vaccinate International Travelers. Vaccine 2017; doi.org/10.1016/j.vaccine.2017.05.090.
65. Duintjer Tebbens RJ, Zimmermann M, Pallansch MA, Thompson KM. Insights from a systematic search for information on designs, costs, and effectiveness of poliovirus environmental surveillance systems. Food and Environmental Virology 2017; doi: 10.1007/s12560-017-9314-4.
66. Thompson KM, Duintjer Tebbens RJ. Lessons from globally-coordinated cessation of serotype 2 oral poliovirus vaccine for the remaining serotypes. J Infect Dis 2017; 216(S1):S168-S175.
67. Thompson KM, Duintjer Tebbens RJ. Lessons From the polio endgame: Overcoming the failure to vaccinate and the role of subpopulations in maintaining transmission. J Infect Dis 2017; 216(S1):S176-S182.