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

Epidemic Thresholds with External Agents

We study the effect of external infection sources on phase transitions in epidemic processes. In particular, we consider an epidemic spreading on a network via the SIS/SIR dynamics, which in addition is aided by external agents - sources unconstrained by the graph, but possessing a limited infection rate or virulence. Such a model captures many existing models of externally aided epidemics, and finds use in many settings - epidemiology, marketing and advertising, network robustness, etc. We provide a detailed characterization of the impact of external agents on epidemic thresholds. In particular, for the SIS model, we show that any external infection strategy with constant virulence either fails to significantly affect the lifetime of an epidemic, or at best, sustains the epidemic for a lifetime which is polynomial in the number of nodes. On the other hand, a random external-infection strategy, with rate increasing linearly in the number of infected nodes, succeeds under some conditions to sustain an exponential epidemic lifetime. We obtain similar sharp thresholds for the SIR model, and discuss the relevance of our results in a variety of settings.Comment: 12 pages, 2 figures (to appear in INFOCOM 2014

Relating Topological Determinants of Complex Networks to Their Spectral Properties: Structural and Dynamical Effects

The largest eigenvalue of a network's adjacency matrix and its associated principal eigenvector are key elements for determining the topological structure and the properties of dynamical processes mediated by it. We present a physically grounded expression relating the value of the largest eigenvalue of a given network to the largest eigenvalue of two network subgraphs, considered as isolated: The hub with its immediate neighbors and the densely connected set of nodes with maximum $K$-core index. We validate this formula showing that it predicts with good accuracy the largest eigenvalue of a large set of synthetic and real-world topologies. We also present evidence of the consequences of these findings for broad classes of dynamics taking place on the networks. As a byproduct, we reveal that the spectral properties of heterogeneous networks built according to the linear preferential attachment model are qualitatively different from those of their static counterparts.Comment: 18 pages, 13 figure

Griffiths phases in infinite-dimensional, non-hierarchical modular networks

Griffiths phases (GPs), generated by the heterogeneities on modular networks, have recently been suggested to provide a mechanism, rid of fine parameter tuning, to explain the critical behavior of complex systems. One conjectured requirement for systems with modular structures was that the network of modules must be hierarchically organized and possess finite dimension. We investigate the dynamical behavior of an activity spreading model, evolving on heterogeneous random networks with highly modular structure and organized non-hierarchically. We observe that loosely coupled modules act as effective rare-regions, slowing down the extinction of activation. As a consequence, we find extended control parameter regions with continuously changing dynamical exponents for single network realizations, preserved after finite size analyses, as in a real GP. The avalanche size distributions of spreading events exhibit robust power-law tails. Our findings relax the requirement of hierarchical organization of the modular structure, which can help to rationalize the criticality of modular systems in the framework of GPs.Comment: 14 pages, 8 figure

Sufficient conditions of endemic threshold on metapopulation networks

In this paper, we focus on susceptible-infected-susceptible dynamics on metapopulation networks, where nodes represent subpopulations, and where agents diffuse and interact. Recent studies suggest that heterogeneous network structure between elements plays an important role in determining the threshold of infection rate at the onset of epidemics, a fundamental quantity governing the epidemic dynamics. We consider the general case in which the infection rate at each node depends on its population size, as shown in recent empirical observations. We first prove that a sufficient condition for the endemic threshold (i.e., its upper bound), previously derived based on a mean-field approximation of network structure, also holds true for arbitrary networks. We also derive an improved condition showing that networks with the rich-club property (i.e., high connectivity between nodes with a large number of links) are more prone to disease spreading. The dependency of infection rate on population size introduces a considerable difference between this upper bound and estimates based on mean-field approximations, even when degree-degree correlations are considered. We verify the theoretical results with numerical simulations.Comment: 32 pages, 5 figure

Griffiths effects of the susceptible-infected-susceptible epidemic model on random power-law networks

We provide numerical evidence for slow dynamics of the susceptible-infected-susceptible model evolving on finite-size random networks with power-law degree distributions. Extensive simulations were done by averaging the activity density over many realizations of networks. We investigated the effects of outliers in both highly fluctuating (natural cutoff) and non-fluctuating (hard cutoff) most connected vertices. Logarithmic and power-law decays in time were found for natural and hard cutoffs, respectively. This happens in extended regions of the control parameter space $\lambda_1<\lambda<\lambda_2$, suggesting Griffiths effects, induced by the topological inhomogeneities. Optimal fluctuation theory considering sample-to-sample fluctuations of the pseudo thresholds is presented to explain the observed slow dynamics. A quasistationary analysis shows that response functions remain bounded at $\lambda_2$. We argue these to be signals of a smeared transition. However, in the thermodynamic limit the Griffiths effects loose their relevancy and have a conventional critical point at $\lambda_c=0$. Since many real networks are composed by heterogeneous and weakly connected modules, the slow dynamics found in our analysis of independent and finite networks can play an important role for the deeper understanding of such systems.Comment: 10 pages, 8 figure