No Arabic abstract
The paradigm for compartment models in epidemiology assumes exponentially distributed incubation and removal times, which is not realistic in actual populations. Commonly used variations with multiple exponentially distributed variables are more flexible, yet do not allow for arbitrary distributions. We present a new formulation, focussing on the SEIR concept that allows to include general distributions of incubation and removal times. We compare the solution to two types of agent-based model simulations, a spatially homogeneous one where infection occurs by proximity, and a model on a scale-free network with varying clustering properties, where the infection between any two agents occurs via their link if it exists. We find good agreement in both cases. Furthermore a family of asymptotic solutions of the equations is found in terms of a logistic curve, which after a non-universal time shift, fits extremely well all the microdynamical simulations. The formulation allows for a simple numerical approach; software in Julia and Python is provided.
The adoption of containment measures to reduce the amplitude of the epidemic peak is a key aspect in tackling the rapid spread of an epidemic. Classical compartmental models must be modified and studied to correctly describe the effects of forced external actions to reduce the impact of the disease. The importance of social structure, such as the age dependence that proved essential in the recent COVID-19 pandemic, must be considered, and in addition, the available data are often incomplete and heterogeneous, so a high degree of uncertainty must be incorporated into the model from the beginning. In this work we address these aspects, through an optimal control formulation of a socially structured epidemic model in presence of uncertain data. After the introduction of the optimal control problem, we formulate an instantaneous approximation of the control that allows us to derive new feedback controlled compartmental models capable of describing the epidemic peak reduction. The need for long-term interventions shows that alternative actions based on the social structure of the system can be as effective as the more expensive global strategy. The timing and intensity of interventions, however, is particularly relevant in the case of uncertain parameters on the actual number of infected people. Simulations related to data from the first wave of the recent COVID-19 outbreak in Italy are presented and discussed.
We develop a new methodology for the efficient computation of epidemic final size distributions for a broad class of Markovian models. We exploit a particular representation of the stochastic epidemic process to derive a method which is both computationally efficient and numerically stable. The algorithms we present are also physically transparent and so allow us to extend this method from the basic SIR model to a model with a phase-type infectious period and another with waning immunity. The underlying theory is applicable to many Markovian models where we wish to efficiently calculate hitting probabilities.
The incubation period of a disease is the time between an initiating pathologic event and the onset of symptoms. For typhoid fever, polio, measles, leukemia and many other diseases, the incubation period is highly variable. Some affected people take much longer than average to show symptoms, leading to a distribution of incubation periods that is right skewed and often approximately lognormal. Although this statistical pattern was discovered more than sixty years ago, it remains an open question to explain its ubiquity. Here we propose an explanation based on evolutionary dynamics on graphs. For simple models of a mutant or pathogen invading a network-structured population of healthy cells, we show that skewed distributions of incubation periods emerge for a wide range of assumptions about invader fitness, competition dynamics, and network structure. The skewness stems from stochastic mechanisms associated with two classic problems in probability theory: the coupon collector and the random walk. Unlike previous explanations that rely crucially on heterogeneity, our results hold even for homogeneous populations. Thus, we predict that two equally healthy individuals subjected to equal doses of equally pathogenic agents may, by chance alone, show remarkably different time courses of disease.
We develop an agent-based model of disease transmission in remote communities in Western Australia. Despite extreme isolation, we show that the movement of people amongst a large number of small but isolated communities has the effect of causing transmission to spread quickly. Significant movement between remote communities, and regional and urban centres allows for infection to quickly spread to and then among these remote communities. Our conclusions are based on two characteristic features of remote communities in Western Australia: (1) high mobility of people amongst these communities, and (2) relatively high proportion of travellers from very small communities to major population centres. In models of infection initiated in the state capital, Perth, these remote communities are collectively and uniquely vulnerable. Our model and analysis does not account for possibly heightened impact due to preexisting conditions, such additional assumptions would only make the projections of this model more dire. We advocate stringent monitoring and control of movement to prevent significant impact on the indigenous population of Western Australia.
We show that precise knowledge of epidemic transmission parameters is not required to build an informative model of the spread of disease. We propose a detailed model of the topology of the contact network under various external control regimes and demonstrate that this is sufficient to capture the salient dynamical characteristics and to inform decisions. Contact between individuals in the community is characterised by a contact graph, the structure of that contact graph is selected to mimic community control measures. Our model of city-level transmission of an infectious agent (SEIR model) characterises spread via a (a) scale-free contact network (no control); (b) a random graph (elimination of mass gatherings); and (c) small world lattice (partial to full lockdown -- social distancing). This model exhibits good qualitative agreement between simulation and data from the 2020 pandemic spread of coronavirus. Estimates of the relevant rate parameters of the SEIR model are obtained and we demonstrate the robustness of our model predictions under uncertainty of those estimates. The social context and utility of this work is identified, contributing to a highly effective pandemic response in Western Australia.