Inferring infection hazard in wildlife populations by linking data across individual and population scales |
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Authors: | Kim M. Pepin Shannon L. Kay Ben D. Golas Susan S. Shriner Amy T. Gilbert Ryan S. Miller Andrea L. Graham Steven Riley Paul C. Cross Michael D. Samuel Mevin B. Hooten Jennifer A. Hoeting James O. Lloyd‐Smith Colleen T. Webb Michael G. Buhnerkempe |
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Affiliation: | 1. National Wildlife Research Center, United States Department of Agriculture, Fort Collins, CO, USA;2. Department of Biology, Colorado State University, Fort Collins, CO, USA;3. Animal and Plant Health Inspection Service, United States Department of Agriculture, Veterinary Services, Fort Collins, CO, USA;4. Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ, USA;5. MRC Centre for Outbreak Analysis and Modelling, Imperial College, London, UK;6. U.S. Geological Survey, Northern Rocky Mountain Science Center, Bozeman, MT, 59715, USA;7. U. S. Geological Survey, Wisconsin Cooperative Wildlife Research Unit, University of Wisconsin, Madison, WI, USA;8. U.S. Geological Survey, Colorado Cooperative Fish and Wildlife Research Unit;9. Departments of Fish, Wildlife, & Conservation Biology and Statistics, Colorado State University, Fort Collins, CO, USA;10. Department of Statistics, Colorado State University, Fort Collins, CO, USA;11. Department of Ecology & Evolutionary Biology, UCLA, Los Angeles, CA, USA |
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Abstract: | Our ability to infer unobservable disease‐dynamic processes such as force of infection (infection hazard for susceptible hosts) has transformed our understanding of disease transmission mechanisms and capacity to predict disease dynamics. Conventional methods for inferring FOI estimate a time‐averaged value and are based on population‐level processes. Because many pathogens exhibit epidemic cycling and FOI is the result of processes acting across the scales of individuals and populations, a flexible framework that extends to epidemic dynamics and links within‐host processes to FOI is needed. Specifically, within‐host antibody kinetics in wildlife hosts can be short‐lived and produce patterns that are repeatable across individuals, suggesting individual‐level antibody concentrations could be used to infer time since infection and hence FOI. Using simulations and case studies (influenza A in lesser snow geese and Yersinia pestis in coyotes), we argue that with careful experimental and surveillance design, the population‐level FOI signal can be recovered from individual‐level antibody kinetics, despite substantial individual‐level variation. In addition to improving inference, the cross‐scale quantitative antibody approach we describe can reveal insights into drivers of individual‐based variation in disease response, and the role of poorly understood processes such as secondary infections, in population‐level dynamics of disease. |
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Keywords: | Antibody antibody kinetics disease hazard force of infection incidence individual‐level variation influenza serosurveillance transmission within‐host |
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