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We prove that it is possible to obtain the exact closure of SIR pairwise epidemic equations on a configuration model network if and only if the degree distribution follows a Poisson, binomial, or negative binomial distribution. The proof relies on establishing the equivalence, for these specific degree distributions, between the closed pairwise model and a dynamical survival analysis (DSA) model that was previously shown to be exact. Specifically, we demonstrate that the DSA model is equivalent to the well-known edge-based Volz model. Using this result, we also provide reductions of the closed pairwise and Volz models to a single equation that involves only susceptibles. This equation has a useful statistical interpretation in terms of times to infection. We provide some numerical examples to illustrate our results.

 

Abstract The 2018–2020 Ebola virus disease epidemic in Democratic Republic of the Congo (DRC) resulted in 3481 cases (probable and confirmed) and 2299 deaths. In this paper, we use a novel statistical method to analyze the individual-level incidence and hospitalization data on DRC Ebola victims. Our analysis suggests that an increase in the rate of quarantine and isolation that has shortened the infectiousness period by approximately one day during the epidemic’s third and final wave was likely responsible for the eventual containment of the outbreak. The analysis further reveals that the total effective population size or the average number of individuals at risk for the disease exposure in three epidemic waves over the period of 24 months was around 16,000–a much smaller number than previously estimated and likely an evidence of at least partial protection of the population at risk through ring vaccination and contact tracing as well as adherence to strict quarantine and isolation policies. 

We study a stochastic compartmental susceptible–infected (SI) epidemic process on a configuration model random graph with a given degree distribution over a finite time interval. We split the population of graph vertices into two compartments, namely, S and I, denoting susceptible and infected vertices, respectively. In addition to the sizes of these two compartments, we keep track of the counts of SI-edges (those connecting a susceptible and an infected vertex) and SS-edges (those connecting two susceptible vertices). We describe the dynamical process in terms of these counts and present a functional central limit theorem (FCLT) for them as the number of vertices in the random graph grows to infinity. The FCLT asserts that the counts, when appropriately scaled, converge weakly to a continuous Gaussian vector semimartingale process in the space of vector-valued càdlàg functions endowed with the Skorokhod topology. We discuss applications of the FCLT in percolation theory and in modelling the spread of computer viruses. We also provide simulation results illustrating the FCLT for some common degree distributions.

 

We present a new method for analysing stochastic epidemic models under minimal assumptions. The method, dubbed dynamic survival analysis (DSA), is based on a simple yet powerful observation, namely that population-level mean-field trajectories described by a system of partial differential equations may also approximate individual-level times of infection and recovery. This idea gives rise to a certain non-Markovian agent-based model and provides an agent-level likelihood function for a random sample of infection and/or recovery times. Extensive numerical analyses on both synthetic and real epidemic data from foot-and-mouth disease in the UK (2001) and COVID-19 in India (2020) show good accuracy and confirm the method’s versatility in likelihood-based parameter estimation. The accompanying software package gives prospective users a practical tool for modelling, analysing and interpreting epidemic data with the help of the DSA approach. 

The Dynamical Survival Analysis (DSA) is a framework for modeling epidemics based on mean field dynamics applied to individual (agent) level history of infection and recovery. Recently, the Dynamical Survival Analysis (DSA) method has been shown to be an effective tool in analyzing complex non-Markovian epidemic processes that are otherwise difficult to handle using standard methods. One of the advantages of Dynamical Survival Analysis (DSA) is its representation of typical epidemic data in a simple although not explicit form that involves solutions of certain differential equations. In this work we describe how a complex non-Markovian Dynamical Survival Analysis (DSA) model may be applied to a specific data set with the help of appropriate numerical and statistical schemes. The ideas are illustrated with a data example of the COVID-19 epidemic in Ohio.

 

Binary classification rules based on a small-sample of high-dimensional data (for instance, gene expression data) are ubiquitous in modern bioinformatics. Constructing such classifiers is challenging due to (a) the complex nature of underlying biological traits, such as gene interactions, and (b) the need for highly interpretable glass-box models. We use the theory of high dimensional model representation (HDMR) to build interpretable low dimensional approximations of the log-likelihood ratio accounting for the effects of each individual gene as well as gene-gene interactions. We propose two algorithms approximating the second order HDMR expansion, and a hypothesis test based on the HDMR formulation to identify significantly dysregulated pairwise interactions. The theory is seen as flexible and requiring only a mild set of assumptions.

We apply our approach to gene expression data from both synthetic and real (breast and lung cancer) datasets comparing it also against several popular state-of-the-art methods. The analyses suggest the proposed algorithms can be used to obtain interpretable prediction rules with high prediction accuracies and to successfully extract significantly dysregulated gene-gene interactions from the data. They also compare favorably against their competitors across multiple synthetic data scenarios.

The proposed HDMR-based approach appears to produce a reliable classifier that additionally allows one to describe how individual genes or gene-gene interactions affect classification decisions. Both real and synthetic data analyses suggest that our methods can be used to identify gene networks with dysregulated pairwise interactions, and are therefore appropriate for differential networks analysis.