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arXiv 1801.01337physics.soc-phmath.DSq-bio.PE
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双层静态-动态可调聚类复用网络上SIR传染病的基于边的房室模型

Edge-based compartmental modelling of an SIR epidemic on a dual-layer static-dynamic multiplex network with tunable clustering

Rosanna C Barnard, Istvan Z Kiss, Luc Berthouze, Joel C Miller

摘要:

在现实世界的人群中,个体之间的联系的持续时间、类型和结构在疾病如何入侵和传播中起着至关重要的作用。在这里,我们将上述的异质性纳入一个模型,考虑一个双层静态-动态复用网络。静态网络层提供可调的集群,并描述了一个人的永久社区结构。动态网络层描述了个体通过不断的边缘重新布线与更广泛群体的成员建立的短暂联系。我们遵循基于边缘的房室模型方法,推导出描述易感-感染-恢复(SIR)传染病传播通过这个多重网络的个人的演变方程。我们推导出基本再生数,衡量在其他易感人群中由单个传染性个体引起的新传染病例的预期数量。我们验证模型方程显示收敛到预先存在的边缘为基础的房室模型方程在极限情况下,并与随机模拟流行病的比较。我们探讨了改变模型参数和多重网络属性对所产生的流行动力学的影响。我们验证了基本的繁殖数绘制其值对相关的最终流行病的大小从模拟和预测模型方程的设置。此外,我们探讨了不同的个人模型参数的基本再生数的影响。最后,我们讨论的意义和解释的模型及其与现有的研究文献。我们强调固有的局限性和潜在的扩展,目前的模型和概述未来的研究考虑,实验和理论。

英文摘要:

The duration, type and structure of connections between individuals in real-world populations play a crucial role in how diseases invade and spread. Here, we incorporate the aforementioned heterogeneities into a model by considering a dual-layer static-dynamic multiplex network. The static network layer affords tunable clustering and describes an individual's permanent community structure. The dynamic network layer describes the transient connections an individual makes with members of the wider population by imposing constant edge rewiring. We follow the edge-based compartmental modelling approach to derive equations describing the evolution of a susceptible - infected - recovered (SIR) epidemic spreading through this multiplex network of individuals. We derive the basic reproduction number, measuring the expected number of new infectious cases caused by a single infectious individual in an otherwise susceptible population. We validate model equations by showing convergence to pre-existing edge-based compartmental model equations in limiting cases and by comparison with stochastically simulated epidemics. We explore the effects of altering model parameters and multiplex network attributes on resultant epidemic dynamics. We validate the basic reproduction number by plotting its value against associated final epidemic sizes measured from simulation and predicted by model equations for a number of setups. Further, we explore the effect of varying individual model parameters on the basic reproduction number. We conclude with a discussion of the significance and interpretation of the model and its relation to existing research literature. We highlight intrinsic limitations and potential extensions of the present model and outline future research considerations, both experimental and theoretical.

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