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A mechanistic model of infection: why duration and intensity of contacts should be included in models of disease spread

BACKGROUND: Mathematical models and simulations of disease spread often assume a constant per-contact transmission probability. This assumption ignores the heterogeneity in transmission probabilities, e.g. due to the varying intensity and duration of potentially contagious contacts. Ignoring such he...

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Detalles Bibliográficos
Autor principal: Smieszek, Timo
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780993/
https://www.ncbi.nlm.nih.gov/pubmed/19919678
http://dx.doi.org/10.1186/1742-4682-6-25
Descripción
Sumario:BACKGROUND: Mathematical models and simulations of disease spread often assume a constant per-contact transmission probability. This assumption ignores the heterogeneity in transmission probabilities, e.g. due to the varying intensity and duration of potentially contagious contacts. Ignoring such heterogeneities might lead to erroneous conclusions from simulation results. In this paper, we show how a mechanistic model of disease transmission differs from this commonly used assumption of a constant per-contact transmission probability. METHODS: We present an exposure-based, mechanistic model of disease transmission that reflects heterogeneities in contact duration and intensity. Based on empirical contact data, we calculate the expected number of secondary cases induced by an infector (i) for the mechanistic model and (ii) under the classical assumption of a constant per-contact transmission probability. The results of both approaches are compared for different basic reproduction numbers R(0). RESULTS: The outcomes of the mechanistic model differ significantly from those of the assumption of a constant per-contact transmission probability. In particular, cases with many different contacts have much lower expected numbers of secondary cases when using the mechanistic model instead of the common assumption. This is due to the fact that the proportion of long, intensive contacts decreases in the contact dataset with an increasing total number of contacts. CONCLUSION: The importance of highly connected individuals, so-called super-spreaders, for disease spread seems to be overestimated when a constant per-contact transmission probability is assumed. This holds particularly for diseases with low basic reproduction numbers. Simulations of disease spread should weight contacts by duration and intensity.