Variance in System Dynamics and Agent Based Modelling Using the SIR Model of Infectious Disease

Classical deterministic simulations of epidemiological processes, such as those based on System Dynamics, produce a single result based on a fixed set of input parameters with no variance between simulations. Input parameters are subsequently modified on these simulations using Monte-Carlo methods, to understand how changes in the input parameters affect the spread of results for the simulation. Agent Based simulations are able to produce different output results on each run based on knowledge of the local interactions of the underlying agents and without making any changes to the input parameters. In this paper we compare the influence and effect of variation within these two distinct simulation paradigms and show that the Agent Based simulation of the epidemiological SIR (Susceptible, Infectious, and Recovered) model is more effective at capturing the natural variation within SIR compared to an equivalent model using System Dynamics with Monte-Carlo simulation. To demonstrate this effect, the SIR model is implemented using both System Dynamics (with Monte-Carlo simulation) and Agent Based Modelling based on previously published empirical data.Comment: Proceedings of the 26th European Conference on Modelling and Simulation (ECMS), Koblenz, Germany, May 2012, pp 9-15, 201

On the spread of epidemics in a closed heterogeneous population

Heterogeneity is an important property of any population experiencing a disease. Here we apply general methods of the theory of heterogeneous populations to the simplest mathematical models in epidemiology. In particular, an SIR (susceptible-infective-removed) model is formulated and analyzed for different sources of heterogeneity. It is shown that a heterogeneous model can be reduced to a homogeneous model with a nonlinear transmission function, which is given in explicit form. The widely used power transmission function is deduced from a heterogeneous model with the initial gamma-distribution of the disease parameters. Therefore, a mechanistic derivation of the phenomenological model, which mimics reality very well, is provided. The equation for the final size of an epidemic for an arbitrary initial distribution is found. The implications of population heterogeneity are discussed, in particular, it is pointed out that usual moment-closure methods can lead to erroneous conclusions if applied for the study of the long-term behavior of the model.Comment: 23 pages, 2 figure

最終感染規模に対する隔離の効果に関する個体群動態モデル

Tohoku University博士（情報科学）thesi

Birth/birth-death processes and their computable transition probabilities with biological applications

Birth-death processes track the size of a univariate population, but many biological systems involve interaction between populations, necessitating models for two or more populations simultaneously. A lack of efficient methods for evaluating finite-time transition probabilities of bivariate processes, however, has restricted statistical inference in these models. Researchers rely on computationally expensive methods such as matrix exponentiation or Monte Carlo approximation, restricting likelihood-based inference to small systems, or indirect methods such as approximate Bayesian computation. In this paper, we introduce the birth(death)/birth-death process, a tractable bivariate extension of the birth-death process. We develop an efficient and robust algorithm to calculate the transition probabilities of birth(death)/birth-death processes using a continued fraction representation of their Laplace transforms. Next, we identify several exemplary models arising in molecular epidemiology, macro-parasite evolution, and infectious disease modeling that fall within this class, and demonstrate advantages of our proposed method over existing approaches to inference in these models. Notably, the ubiquitous stochastic susceptible-infectious-removed (SIR) model falls within this class, and we emphasize that computable transition probabilities newly enable direct inference of parameters in the SIR model. We also propose a very fast method for approximating the transition probabilities under the SIR model via a novel branching process simplification, and compare it to the continued fraction representation method with application to the 17th century plague in Eyam. Although the two methods produce similar maximum a posteriori estimates, the branching process approximation fails to capture the correlation structure in the joint posterior distribution

A non-standard numerical scheme for an age-of-infection epidemic model

We propose a numerical method for approximating integro-differential equations arising in age-of-infection epidemic models. The method is based on a non-standard finite differences approximation of the integral term appearing in the equation. The study of convergence properties and the analysis of the qualitative behavior of the numerical solution show that it preserves all the basic properties of the continuous model with no restrictive conditions on the step-length $h$ of integration and that it recovers the continuous dynamic as $h$ tends to zero.Comment: 17 pages, 3 figure

A systematic procedure for incorporating separable static heterogeneity into compartmental epidemic models

In this paper, we show how to modify a compartmental epidemic model, without changing the dimension, such that separable static heterogeneity is taken into account. The derivation is based on the Kermack-McKendrick renewal equation

Stochastic epidemic models with varying infectivity and susceptibility

We study an individual-based stochastic epidemic model in which infected individuals become susceptible again following each infection. In contrast to classical compartment models, after each infection, the infectivity is a random function of the time elapsed since one's infection. Similarly, recovered individuals become gradually susceptible after some time according to a random susceptibility function. We study the large population asymptotic behaviour of the model, by proving a functional law of large numbers (FLLN) and investigating the endemic equilibria properties of the limit. The limit depends on the law of the susceptibility random functions but only on the mean infectivity functions. The FLLN is proved by constructing a sequence of i.i.d. auxiliary processes and adapting the approach from the theory of propagation of chaos. The limit is a generalisation of a PDE model introduced by Kermack and McKendrick, and we show how this PDE model can be obtained as a special case of our FLLN limit.% for a particular set of infectivity and susceptibility random functions and initial conditions. For the endemic equilibria, if $R_0$ is lower than (or equal to) some threshold, the epidemic does not last forever and eventually disappears from the population, while if $R_0$ is larger than this threshold, the epidemic will not disappear and there exists an endemic equilibrium. The value of this threshold turns out to depend on the harmonic mean of the susceptibility a long time after an infection, a fact which was not previously known