scholarly journals A model for the co-evolution of dynamic social networks and infectious disease dynamics

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Hendrik Nunner ◽  
Vincent Buskens ◽  
Mirjam Kretzschmar

AbstractRecent research shows an increasing interest in the interplay of social networks and infectious diseases. Many studies either neglect explicit changes in health behavior or consider networks to be static, despite empirical evidence that people seek to distance themselves from diseases in social networks. We propose an adaptable steppingstone model that integrates theories of social network formation from sociology, risk perception from health psychology, and infectious diseases from epidemiology. We argue that networking behavior in the context of infectious diseases can be described as a trade-off between the benefits, efforts, and potential harm a connection creates. Agent-based simulations of a specific model case show that: (i) high (perceived) health risks create strong social distancing, thus resulting in low epidemic sizes; (ii) small changes in health behavior can be decisive for whether the outbreak of a disease turns into an epidemic or not; (iii) high benefits for social connections create more ties per agent, providing large numbers of potential transmission routes and opportunities for the disease to travel faster, and (iv) higher costs of maintaining ties with infected others reduce final size of epidemics only when benefits of indirect ties are relatively low. These findings suggest a complex interplay between social network, health behavior, and infectious disease dynamics. Furthermore, they contribute to solving the issue that neglect of explicit health behavior in models of disease spread may create mismatches between observed transmissibility and epidemic sizes of model predictions.

2021 ◽  
Author(s):  
Hendrik Nunner ◽  
Vincent Buskens ◽  
Mirjam Kretzschmar

Abstract Recent research shows an increasing interest in the interplay of social networks and infectious diseases. Many studies either neglect explicit changes in health behavior or consider networks to be static, despite empirical evidence that people seek to distance themselves from diseases in social networks. We propose an adaptable steppingstone model that integrates theories of social network formation from sociology, risk perception from health psychology, and infectious diseases from epidemiology. We argue that networking behavior in the context of infectious diseases can be described as a trade-off between the benefits, efforts, and potential harm a connection creates. Agent-based simulations using a generic model implementation show that: (i) high (perceived) health risks create strong social distancing, thus resulting in low epidemic sizes, (ii) small changes in health behavior can be decisive for whether the outbreak of a disease turns into an epidemic or not, (iii) high benefits for social connections create more ties per agent, providing large numbers of potential transmission routes and opportunities for the disease to travel faster, and (iv) higher costs of maintaining ties with infected others reduce final size of epidemics only when benefits of indirect ties are relatively low. These findings suggest a complex interplay between social network, health behavior, and infectious disease dynamics. Furthermore, they contribute to solving the issue that neglect of explicit health behavior in models of disease spread may create mismatches between observed transmissibility and epidemic sizes of model predictions.


2021 ◽  
Vol 118 (18) ◽  
pp. e2007488118
Author(s):  
Daniel T. Citron ◽  
Carlos A. Guerra ◽  
Andrew J. Dolgert ◽  
Sean L. Wu ◽  
John M. Henry ◽  
...  

Newly available datasets present exciting opportunities to investigate how human population movement contributes to the spread of infectious diseases across large geographical distances. It is now possible to construct realistic models of infectious disease dynamics for the purposes of understanding global-scale epidemics. Nevertheless, a remaining unanswered question is how best to leverage the new data to parameterize models of movement, and whether one’s choice of movement model impacts modeled disease outcomes. We adapt three well-studied models of infectious disease dynamics, the susceptible–infected–recovered model, the susceptible–infected–susceptible model, and the Ross–Macdonald model, to incorporate either of two candidate movement models. We describe the effect that the choice of movement model has on each disease model’s results, finding that in all cases, there are parameter regimes where choosing one movement model instead of another has a profound impact on epidemiological outcomes. We further demonstrate the importance of choosing an appropriate movement model using the applied case of malaria transmission and importation on Bioko Island, Equatorial Guinea, finding that one model produces intelligible predictions of R0, whereas the other produces nonsensical results.


2010 ◽  
Vol 7 (50) ◽  
pp. 1247-1256 ◽  
Author(s):  
Sebastian Funk ◽  
Marcel Salathé ◽  
Vincent A. A. Jansen

Human behaviour plays an important role in the spread of infectious diseases, and understanding the influence of behaviour on the spread of diseases can be key to improving control efforts. While behavioural responses to the spread of a disease have often been reported anecdotally, there has been relatively little systematic investigation into how behavioural changes can affect disease dynamics. Mathematical models for the spread of infectious diseases are an important tool for investigating and quantifying such effects, not least because the spread of a disease among humans is not amenable to direct experimental study. Here, we review recent efforts to incorporate human behaviour into disease models, and propose that such models can be broadly classified according to the type and source of information which individuals are assumed to base their behaviour on, and according to the assumed effects of such behaviour. We highlight recent advances as well as gaps in our understanding of the interplay between infectious disease dynamics and human behaviour, and suggest what kind of data taking efforts would be helpful in filling these gaps.


2020 ◽  
Author(s):  
Daniel T. Citron ◽  
Carlos A. Guerra ◽  
Andrew J. Dolgert ◽  
Sean L. Wu ◽  
John M. Henry ◽  
...  

Newly available data sets present an exciting opportunity to investigate how human population movement contributes to the spread of infectious diseases across large geographical distances. It is now possible to construct realistic models of infectious disease dynamics for the purposes of understanding global-scale epidemics. Nevertheless, a remaining unanswered question is how best to leverage the new data to parameterize models of movement, and whether one’s choice of movement model impacts modeled disease outcomes. We adapt three well-studied models of infectious disease dynamics, the SIR model; the SIS model; and the Ross-Macdonald model, to incorporate either of two candidate movement models. We describe the effect that the choice of movement model has on each disease model’s results, finding that in all cases there are parameter regimes where choosing one movement model instead of another has a profound impact on epidemiological outcomes. We further demonstrate the importance of choosing an appropriate movement model using the applied case of malaria transmission and importation on Bioko Island, Equatorial Guinea, finding that one model produces intelligible predictions of R0 while the other produces nonsensical results.


Author(s):  
I. Abdul Jalil ◽  
A. R. Abdul Rasam

Abstract. The movement of individuals between specific locations and the different group contacts of people is essential to predict the future movement and interaction pattern of infectious diseases. Previous studies have shown major factor of infectious disease spread comes from human mobility because a complex and dynamic network of spatial interactions between locations such as the mobility formed by the daily activity of people from place to place. To better understand the such human mobility behaviour, innovative methods are required to depict and analyse their structures by using social network analysis (SNA). This paper aims to investigate the social network structure of selected tuberculosis (TB) case in Klang, Selangor as actors (nodes), and then human mobility (home-work place) data as edge generally used to investigate social network mobility structures and analyse relation among the nodes and study their edges in term of their network centrality. The main finding has revealed that the higher the centrality (degree and betweenness) of a node in the network structure, the higher the chance the node influencing the TB spread in the whole network, after comparing the network graph result with the geographic information system (GIS) mapping approach. Most of the result share the similar result where most of high infection of TB are located in urban and crowded areas. The SNA is a practical knowledge of the social system and contact structure of a community that can therefore provide crucial information to predict outbreaks of infectious diseases in a dynamic spatial phenomena.


2013 ◽  
Vol 280 (1766) ◽  
pp. 20130763 ◽  
Author(s):  
Benjamin D. Dalziel ◽  
Babak Pourbohloul ◽  
Stephen P. Ellner

The epidemic dynamics of infectious diseases vary among cities, but it is unclear how this is caused by patterns of infectious contact among individuals. Here, we ask whether systematic differences in human mobility patterns are sufficient to cause inter-city variation in epidemic dynamics for infectious diseases spread by casual contact between hosts. We analyse census data on the mobility patterns of every full-time worker in 48 Canadian cities, finding a power-law relationship between population size and the level of organization in mobility patterns, where in larger cities, a greater fraction of workers travel to work in a few focal locations. Similarly sized cities also vary in the level of organization in their mobility patterns, equivalent on average to the variation expected from a 2.64-fold change in population size. Systematic variation in mobility patterns is sufficient to cause significant differences among cities in infectious disease dynamics—even among cities of the same size—according to an individual-based model of airborne pathogen transmission parametrized with the mobility data. This suggests that differences among cities in host contact patterns are sufficient to drive differences in infectious disease dynamics and provides a framework for testing the effects of host mobility patterns in city-level disease data.


2020 ◽  
Vol 6 (3) ◽  
pp. 159-161
Author(s):  
Tyler G. James ◽  
Catherine A. Lippi

Infectious diseases, including zoonotic infectious diseases, are some of the leading causes of the global burden of diseases. Public health education/promotion specialists are specifically trained in methods and theory to deliver risk communication that can help decrease the transmissibility, morbidity, and mortality of infectious diseases. However, the limited training of health educators in infectious disease dynamics represents a critical barrier for health educators wishing to engage in this work. In this commentary, we describe the importance of health education/promotion specialists being trained on infectious disease dynamics to engage in effective science and health communication locally and globally.


2009 ◽  
Vol 78 (5) ◽  
pp. 1015-1022 ◽  
Author(s):  
Sarah E. Perkins ◽  
Francesca Cagnacci ◽  
Anna Stradiotto ◽  
Daniele Arnoldi ◽  
Peter J. Hudson

2017 ◽  
Vol 372 (1719) ◽  
pp. 20160454 ◽  
Author(s):  
Ronan F. Arthur ◽  
Emily S. Gurley ◽  
Henrik Salje ◽  
Laura S. P. Bloomfield ◽  
James H. Jones

Human factors, including contact structure, movement, impact on the environment and patterns of behaviour, can have significant influence on the emergence of novel infectious diseases and the transmission and amplification of established ones. As anthropogenic climate change alters natural systems and global economic forces drive land-use and land-cover change, it becomes increasingly important to understand both the ecological and social factors that impact infectious disease outcomes for human populations. While the field of disease ecology explicitly studies the ecological aspects of infectious disease transmission, the effects of the social context on zoonotic pathogen spillover and subsequent human-to-human transmission are comparatively neglected in the literature. The social sciences encompass a variety of disciplines and frameworks for understanding infectious diseases; however, here we focus on four primary areas of social systems that quantitatively and qualitatively contribute to infectious diseases as social–ecological systems. These areas are social mixing and structure, space and mobility, geography and environmental impact, and behaviour and behaviour change. Incorporation of these social factors requires empirical studies for parametrization, phenomena characterization and integrated theoretical modelling of social–ecological interactions. The social–ecological system that dictates infectious disease dynamics is a complex system rich in interacting variables with dynamically significant heterogeneous properties. Future discussions about infectious disease spillover and transmission in human populations need to address the social context that affects particular disease systems by identifying and measuring qualitatively important drivers. This article is part of the themed issue ‘Opening the black box: re-examining the ecology and evolution of parasite transmission’.


2019 ◽  
Author(s):  
Amy E. Kendig ◽  
Elizabeth T. Borer ◽  
Emily N. Boak ◽  
Tashina C. Picard ◽  
Eric W. Seabloom

AbstractInteractions among co-infecting pathogens are common across host taxa and can affect infectious disease dynamics. Host nutrition can mediate these among-pathogen interactions, altering the establishment and growth of pathogens within hosts. It is unclear, however, how nutrition-mediated among-pathogen interactions affect transmission and the spread of disease through populations. We manipulated the nitrogen (N) and phosphorus (P) supplies to oat plants in growth chambers and evaluated interactions between two aphid-vectored Barley and Cereal Yellow Dwarf Viruses: PAV and RPV. We quantified the effect of each virus on the other’s establishment, within-plant density, and transmission. Co-inoculation significantly increased PAV density when N and P supplies were low and tended to increase RPV density when N supply was high. Co-infection increased PAV transmission when N and P supplies were low and tended to increase RPV transmission when N supply was high. Despite the parallels between the effects of among-pathogen interactions on density and transmission, changes in virus density only partially explained changes in transmission, suggesting that virus density–independent processes contribute to transmission. A mathematical model describing the spread of two viruses through a plant population, parameterized with empirically derived transmission values, demonstrated that nutrition-mediated among-pathogen interactions could affect disease spread. Interactions that altered transmission through virus density–independent processes determined overall disease dynamics. Our work suggests that host nutrition alters disease spread through among-pathogen interactions that modify transmission.


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