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A Computational Simulation Model for Predicting Infectious Disease Spread using the Evolving Contact Network Algorithm

Abstract
Commonly used simulation models for predicting outbreaks of re-emerging infectious diseases (EIDs) take an individual-level or a population-level approach to modeling contact dynamics. These approaches are a trade-off between the ability to incorporate individual-level dynamics and computational efficiency. Agent-based network models (ABNM) use an individual-level approach by simulating the entire population and its contact structure, which increases the ability of adding detailed individual-level characteristics. However, as this method is computationally expensive, ABNMs use scaled-down versions of the full population, which are unsuitable for low prevalence diseases as the number of infected cases would become negligible during scaling-down. Compartmental models use differential equations to simulate population-level features, which is computationally inexpensive and can model full-scale populations. However, as the compartmental model framework assumes random mixing between people, it is not suitable for diseases where the underlying contact structures are a significant feature of disease epidemiology. Therefore, current methods are unsuitable for simulating diseases that have low prevalence and where the contact structures are significant. The conceptual framework for a new simulation method, Evolving Contact Network Algorithm (ECNA), was recently proposed to address the above gap. The ECNA combines the attributes of ABNM and compartmental modeling. It generates a contact network of only infected persons and their immediate contacts, and evolves the network as new persons become infected. The conceptual framework of the ECNA is promising for application to diseases with low prevalence and where contact structures are significant. This thesis develops and tests different algorithms to advance the computational capabilities of the ECNA and its flexibility to model different network settings. These features are key components that determine the feasibility of ECNA for application to disease prediction. Results indicate that the ECNA is nearly 20 times faster than ABNM when simulating a population of size 150,000 and flexible for modeling networks with two contact layers and communities. Considering uncertainties in epidemiological features and origin of future EIDs, there is a significant need for a computationally efficient method that is suitable for analyses of a range of potential EIDs at a global scale. This work holds promise towards the development of such a model.
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