Significance This study infers probabilistic infection routes of a vector-borne disease, by modeling internal dynamics of metapopulations driven by human mobility as multivariate stochastic processes. In this way, our proposed… Click to show full abstract
Significance This study infers probabilistic infection routes of a vector-borne disease, by modeling internal dynamics of metapopulations driven by human mobility as multivariate stochastic processes. In this way, our proposed model uncovers the self-excitation and mutual excitation nature of disease spread across a heterogeneous social system with rich context. Our model is a general extension of networked Hawkes processes, providing flexibilities to add constraints (presence of diffusion medium) and to use domain knowledge (cross-metapopulation connectivity), enabling covering of direct and indirect diffusion processes such as contact-based and vector-borne disease spread. Our model is readily applicable to a wide range of intragroup and intergroup diffusion processes in social and natural systems and can infer probabilistic causality between discrete events. Diffusion processes are governed by external triggers and internal dynamics in complex systems. Timely and cost-effective control of infectious disease spread critically relies on uncovering underlying diffusion mechanisms, which is challenging due to invisible infection pathways and time-evolving intensity of infection cases. Here, we propose a new diffusion framework for stochastic processes, which models disease spread across metapopulations by incorporating human mobility as topological pathways in a heterogeneous social system. We apply Bayesian inference with the stochastic Expectation–Maximization algorithm to quantify underlying diffusion dynamics in terms of exogeneity and endogeneity and estimate cross-regional infection flow based on Granger causality. The effectiveness of our proposed model is shown by using comprehensive simulation procedures (robustness tests with noisy data considering missing or delayed human case reporting in real situations) and by applying the model to real data from 15-y dengue outbreaks in Australia.
               
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