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Inferring infection hazard in wildlife populations by linking data across individual and population scales.

Identifieur interne : 000107 ( Main/Exploration ); précédent : 000106; suivant : 000108

Inferring infection hazard in wildlife populations by linking data across individual and population scales.

Auteurs : Kim M. Pepin [États-Unis] ; Shannon L. Kay [États-Unis] ; Ben D. Golas [États-Unis] ; Susan S. Shriner [États-Unis] ; Amy T. Gilbert [États-Unis] ; Ryan S. Miller [États-Unis] ; Andrea L. Graham [États-Unis] ; Steven Riley [Royaume-Uni] ; Paul C. Cross [États-Unis] ; Michael D. Samuel [États-Unis] ; Mevin B. Hooten [États-Unis] ; Jennifer A. Hoeting [États-Unis] ; James O. Lloyd-Smith [États-Unis] ; Colleen T. Webb [États-Unis] ; Michael G. Buhnerkempe [États-Unis]

Source :

RBID : pubmed:28090753

Descripteurs français

English descriptors

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.

DOI: 10.1111/ele.12732
PubMed: 28090753
PubMed Central: PMC7163542


Affiliations:


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Le document en format XML

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<name sortKey="Miller, Ryan S" sort="Miller, Ryan S" uniqKey="Miller R" first="Ryan S" last="Miller">Ryan S. Miller</name>
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<name sortKey="Graham, Andrea L" sort="Graham, Andrea L" uniqKey="Graham A" first="Andrea L" last="Graham">Andrea L. Graham</name>
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<name sortKey="Riley, Steven" sort="Riley, Steven" uniqKey="Riley S" first="Steven" last="Riley">Steven Riley</name>
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<nlm:affiliation>MRC Centre for Outbreak Analysis and Modelling, Imperial College, London, UK.</nlm:affiliation>
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<name sortKey="Cross, Paul C" sort="Cross, Paul C" uniqKey="Cross P" first="Paul C" last="Cross">Paul C. Cross</name>
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<term>Age Factors (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Antibodies, Viral (analysis)</term>
<term>Computer Simulation (MeSH)</term>
<term>Coyotes (MeSH)</term>
<term>Cross-Sectional Studies (MeSH)</term>
<term>Ducks (MeSH)</term>
<term>Epidemiologic Methods (veterinary)</term>
<term>Geese (MeSH)</term>
<term>Influenza A virus (physiology)</term>
<term>Influenza in Birds (epidemiology)</term>
<term>Influenza in Birds (virology)</term>
<term>Longitudinal Studies (MeSH)</term>
<term>Northwest Territories (epidemiology)</term>
<term>Plague (epidemiology)</term>
<term>Plague (microbiology)</term>
<term>Plague (veterinary)</term>
<term>Poultry Diseases (epidemiology)</term>
<term>Poultry Diseases (virology)</term>
<term>Prevalence (MeSH)</term>
<term>Risk Assessment (methods)</term>
<term>Seroepidemiologic Studies (MeSH)</term>
<term>Yersinia pestis (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Animaux (MeSH)</term>
<term>Anticorps antiviraux (analyse)</term>
<term>Appréciation des risques (méthodes)</term>
<term>Canards (MeSH)</term>
<term>Coyotes (MeSH)</term>
<term>Facteurs âges (MeSH)</term>
<term>Grippe chez les oiseaux (virologie)</term>
<term>Grippe chez les oiseaux (épidémiologie)</term>
<term>Maladies de la volaille (virologie)</term>
<term>Maladies de la volaille (épidémiologie)</term>
<term>Méthodes épidémiologiques (médecine vétérinaire)</term>
<term>Oies (MeSH)</term>
<term>Peste (microbiologie)</term>
<term>Peste (médecine vétérinaire)</term>
<term>Peste (épidémiologie)</term>
<term>Prévalence (MeSH)</term>
<term>Simulation numérique (MeSH)</term>
<term>Territoires du Nord-Ouest (Canada) (épidémiologie)</term>
<term>Virus de la grippe A (physiologie)</term>
<term>Yersinia pestis (physiologie)</term>
<term>Études longitudinales (MeSH)</term>
<term>Études séroépidémiologiques (MeSH)</term>
<term>Études transversales (MeSH)</term>
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<term>Antibodies, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="analyse" xml:lang="fr">
<term>Anticorps antiviraux</term>
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<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en">
<term>Influenza in Birds</term>
<term>Northwest Territories</term>
<term>Plague</term>
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<div type="abstract" xml:lang="en">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.</div>
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<Title>Ecology letters</Title>
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<ArticleTitle>Inferring infection hazard in wildlife populations by linking data across individual and population scales.</ArticleTitle>
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<AbstractText>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.</AbstractText>
<CopyrightInformation>© 2017 John Wiley & Sons Ltd/CNRS.</CopyrightInformation>
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<LastName>Pepin</LastName>
<ForeName>Kim M</ForeName>
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<Affiliation>National Wildlife Research Center, United States Department of Agriculture, 4101 Laporte Ave., Fort Collins, CO, 80521, USA.</Affiliation>
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<ForeName>Shannon L</ForeName>
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<LastName>Golas</LastName>
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<Affiliation>Department of Biology, Colorado State University, Fort Collins, CO, 80523, USA.</Affiliation>
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<ForeName>Susan S</ForeName>
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<LastName>Lloyd-Smith</LastName>
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<LastName>Webb</LastName>
<ForeName>Colleen T</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Biology, Colorado State University, Fort Collins, CO, 80523, USA.</Affiliation>
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<LastName>Buhnerkempe</LastName>
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<Affiliation>Department of Ecology & Evolutionary Biology, UCLA, Los Angeles, CA, 90095, USA.</Affiliation>
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