Epidemic processes in complex networks

In recent years the research community has accumulated overwhelming evidence for the emergence of complex and heterogeneous connectivity patterns in a wide range of biological and sociotechnical systems. The complex properties of real-world networks have a profound impact on the behavior of equilibrium and nonequilibrium phenomena occurring in various systems, and the study of epidemic spreading is central to our understanding of the unfolding of dynamical processes in complex networks. The theoretical analysis of epidemic spreading in heterogeneous networks requires the development of novel analytical frameworks, and it has produced results of conceptual and practical relevance. A coherent and comprehensive review of the vast research activity concerning epidemic processes is presented, detailing the successful theoretical approaches as well as making their limits and assumptions clear. Physicists, mathematicians, epidemiologists, computer, and social scientists share a common interest in studying epidemic spreading and rely on similar models for the description of the diffusion of pathogens, knowledge, and innovation. For this reason, while focusing on the main results and the paradigmatic models in infectious disease modeling, the major results concerning generalized social contagion processes are also presented. Finally, the research activity at the forefront in the study of epidemic spreading in coevolving, coupled, and time-varying networks is reported.Comment: 62 pages, 15 figures, final versio

Network centrality: an introduction

Centrality is a key property of complex networks that influences the behavior of dynamical processes, like synchronization and epidemic spreading, and can bring important information about the organization of complex systems, like our brain and society. There are many metrics to quantify the node centrality in networks. Here, we review the main centrality measures and discuss their main features and limitations. The influence of network centrality on epidemic spreading and synchronization is also pointed out in this chapter. Moreover, we present the application of centrality measures to understand the function of complex systems, including biological and cortical networks. Finally, we discuss some perspectives and challenges to generalize centrality measures for multilayer and temporal networks.Comment: Book Chapter in "From nonlinear dynamics to complex systems: A Mathematical modeling approach" by Springe

Pair quenched mean-field theory for the susceptible-infected-susceptible model on complex networks

We present a quenched mean-field (QMF) theory for the dynamics of the susceptible-infected-susceptible (SIS) epidemic model on complex networks where dynamical correlations between connected vertices are taken into account by means of a pair approximation. We present analytical expressions of the epidemic thresholds in the star and wheel graphs and in random regular networks. For random networks with a power law degree distribution, the thresholds are numerically determined via an eigenvalue problem. The pair and one-vertex QMF theories yield the same scaling for the thresholds as functions of the network size. However, comparisons with quasi-stationary simulations of the SIS dynamics on large networks show that the former is quantitatively much more accurate than the latter. Our results demonstrate the central role played by dynamical correlations on the epidemic spreading and introduce an efficient way to theoretically access the thresholds of very large networks that can be extended to dynamical processes in general.Comment: 6 pages, 6 figure

Dynamic Behavior of Interacting between Epidemics and Cascades on Heterogeneous Networks

Epidemic spreading and cascading failure are two important dynamical processes over complex networks. They have been investigated separately for a long history. But in the real world, these two dynamics sometimes may interact with each other. In this paper, we explore a model combined with SIR epidemic spreading model and local loads sharing cascading failure model. There exists a critical value of tolerance parameter that whether the epidemic with high infection probability can spread out and infect a fraction of the network in this model. When the tolerance parameter is smaller than the critical value, cascading failure cuts off abundant of paths and blocks the spreading of epidemic locally. While the tolerance parameter is larger than the critical value, epidemic spreads out and infects a fraction of the network. A method for estimating the critical value is proposed. In simulation, we verify the effectiveness of this method in Barab\'asi-Albert (BA) networks

Optimized Gillespie algorithms for the simulation of Markovian epidemic processes on large and heterogeneous networks

Numerical simulation of continuous-time Markovian processes is an essential and widely applied tool in the investigation of epidemic spreading on complex networks. Due to the high heterogeneity of the connectivity structure through which epidemics is transmitted, efficient and accurate implementations of generic epidemic processes are not trivial and deviations from statistically exact prescriptions can lead to uncontrolled biases. Based on the Gillespie algorithm (GA), in which only steps that change the state are considered, we develop numerical recipes and describe their computer implementations for statistically exact and computationally efficient simulations of generic Markovian epidemic processes aiming at highly heterogeneous and large networks. The central point of the recipes investigated here is to include phantom processes, that do not change the states but do count for time increments. We compare the efficiencies for the susceptible-infected-susceptible, contact process and susceptible-infected-recovered models, that are particular cases of a generic model considered here. We numerically confirm that the simulation outcomes of the optimized algorithms are statistically indistinguishable from the original GA and can be several orders of magnitude more efficient.Comment: 12 pages, 9 figure