Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4495831 | Journal of Theoretical Biology | 2016 | 10 Pages |
•We create an agent based network model that simulates an epidemic.•We combine population decisions for vaccination and non-pharmaceutical interventions.•Vaccination mitigates epidemic final size effectively for high transmission rates.•Non-pharmaceutical interventions compensate for delays in vaccine availability.•Non-pharmaceutical interventions can lower vaccine uptake and reduce epidemic size.
Mathematical models of the interplay between disease dynamics and human behavioural dynamics can improve our understanding of how diseases spread when individuals adapt their behaviour in response to an epidemic. Accounting for behavioural mechanisms that determine uptake of infectious disease interventions such as vaccination and non-pharmaceutical interventions (NPIs) can significantly alter predicted health outcomes in a population. However, most previous approaches that model interactions between human behaviour and disease dynamics have modelled behaviour of these two interventions separately. Here, we develop and analyze an agent based network model to gain insights into how behaviour toward both interventions interact adaptively with disease dynamics (and therefore, indirectly, with one another) during the course of a single epidemic where an SIRV infection spreads through a contact network. In the model, individuals decide to become vaccinated and/or practice NPIs based on perceived infection prevalence (locally or globally) and on what other individuals in the network are doing. We find that introducing adaptive NPI behaviour lowers vaccine uptake on account of behavioural feedbacks, and also decreases epidemic final size. When transmission rates are low, NPIs alone are as effective in reducing epidemic final size as NPIs and vaccination combined. Also, NPIs can compensate for delays in vaccine availability by hindering early disease spread, decreasing epidemic size significantly compared to the case where NPI behaviour does not adapt to mitigate early surges in infection prevalence. We also find that including adaptive NPI behaviour strongly mitigates the vaccine behavioural feedbacks that would otherwise result in higher vaccine uptake at lower vaccine efficacy as predicted by most previous models, and the same feedbacks cause epidemic final size to remain approximately constant across a broad range of values for vaccine efficacy. Finally, when individuals use local information about others’ behaviour and infection prevalence, instead of population-level information, infection is controlled more efficiently through ring vaccination, and this is reflected in the time evolution of pair correlations on the network. This model shows that accounting for both adaptive NPI behaviour and adaptive vaccinating behaviour regarding social effects and infection prevalence can result in qualitatively different predictions than if only one type of adaptive behaviour is modelled.