There is a continuing debate on relative benefits of various mitigation and suppression strategies aimed to control the spread of COVID-19. Here we report the results of agent-based modelling using a fine-grained computational simulation of the ongoing COVID-19 pandemic in Australia. This model is calibrated to match key characteristics of COVID-19 transmission. An important calibration outcome is the age-dependent fraction of symptomatic cases, with this fraction for children found to be one-fifth of such fraction for adults. We apply the model to compare several intervention strategies, including restrictions on international air travel, case isolation, home quarantine, social distancing with varying levels of compliance, and school closures. School closures are not found to bring decisive benefits unless coupled with high level of social distancing compliance. We report several trade-offs, and an important transition across the levels of social distancing compliance, in the range between 70% and 80% levels, with compliance at the 90% level found to control the disease within 13–14 weeks, when coupled with effective case isolation and international travel restrictions.

In this paper we present AceMod, an agent-based modelling framework for studying influenza epidemics in Australia. The simulator is designed to analyse the spatiotemporal spread of contagion and influenza spatial synchrony across the nation. The individual-based epidemiological model accounts for mobility (worker and student commuting) patterns and human interactions derived from the 2006 Australian census and other national data sources. The high-precision simulation comprises 19.8 million stochastically generated software agents and traces the dynamics of influenza viral infection and transmission at several scales. Using this approach, we are able to synthesise epidemics in Australia with varying outbreak locations and severity. For each scenario, we investigate the spatiotemporal profiles of these epidemics, both qualitatively and quantitatively, via incidence curves, prevalence choropleths, and epidemic synchrony. This analysis exemplifies the nature of influenza pandemics within Australia and facilitates future planning of effective intervention, mitigation and crisis management strategies.

Simulations associate urbanization with earlier peaks, higher peak prevalence, and shifting bimodality of pandemics in Australia.

When new, highly infectious strains of influenza emerge, global pandemics can occur before an effective vaccine is developed. Without a strain-specific vaccine, pandemics can only be mitigated by employing combinations of low-efficacy pre-pandemic vaccines and reactive response measures that are carried out as the pandemic unfolds. Unfortunately, the application of reactive interventions can lead to unintended consequences that may exacerbate unpredictable spreading dynamics and cause more drawn-out epidemics. Here, we employ a detailed model of pandemic influenza in Australia to simulate the combination of pre-pandemic vaccination and reactive antiviral prophylaxis. This study focuses on population-level coupling effects between the respective methods, and the associated spatio-temporal fluctuations in pandemic dynamics produced by reactive strategies. Our results show that combining strategies can produce either mutual improvement of performance or interference that reduces the effectiveness of each strategy when they are used together. We demonstrate that these coupling effects between intervention strategies are extremely sensitive to delay times, compliance rates and the type of contact targeting used to administer prophylaxis.

We present a novel approach to the study of epidemics on networks as thermodynamic phenomena, quantifying the thermodynamic efficiency of contagions, considered as distributed computational processes. Modelling SIS dynamics on a contact network statistical-mechanically, we follow the Maximum Entropy principle to obtain steady state distributions and derive, under certain assumptions, relevant thermodynamic quantities both analytically and numerically. In particular, we obtain closed form solutions for some cases, while interpreting key epidemic variables, such as the reproductive ratio R0 of a SIS model, in a statistical mechanical setting. On the other hand, we consider configuration and free entropy, as well as the Fisher Information, in the epidemiological context. This allowed us to identify criticality and distinct phases of epidemic processes. For each of the considered thermodynamic quantities, we compare the analytical solutions informed by the Maximum Entropy principle with the numerical estimates for SIS epidemics simulated on Watts-Strogatz random graphs.