| Literature DB >> 34328080 |
Ewan Colman1,2, Vittoria Colizza3, Ephraim M Hanks4, David P Hughes5, Shweta Bansal1.
Abstract
Humans and other group-living animals tend to distribute their social effort disproportionately. Individuals predominantly interact with a small number of close companions while maintaining weaker social bonds with less familiar group members. By incorporating this behavior into a mathematical model, we find that a single parameter, which we refer to as social fluidity, controls the rate of social mixing within the group. Large values of social fluidity correspond to gregarious behavior, whereas small values signify the existence of persistent bonds between individuals. We compare the social fluidity of 13 species by applying the model to empirical human and animal social interaction data. To investigate how social behavior influences the likelihood of an epidemic outbreak, we derive an analytical expression of the relationship between social fluidity and the basic reproductive number of an infectious disease. For species that form more stable social bonds, the model describes frequency-dependent transmission that is sensitive to changes in social fluidity. As social fluidity increases, animal-disease systems become increasingly density-dependent. Finally, we demonstrate that social fluidity is a stronger predictor of disease outcomes than both group size and connectivity, and it provides an integrated framework for both density-dependent and frequency-dependent transmission.Entities:
Keywords: animal behaviour; computational biology; density dependence; epidemiology; frequency dependence; global health; infectious disease; mathematical modelling; none; sociality; systems biology
Mesh:
Year: 2021 PMID: 34328080 PMCID: PMC8324292 DOI: 10.7554/eLife.62177
Source DB: PubMed Journal: Elife ISSN: 2050-084X Impact factor: 8.713