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

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

Multiple phase transitions of the susceptible-infected-susceptible epidemic model on complex networks

The epidemic threshold of the susceptible-infected-susceptible (SIS) dynamics on random networks having a power law degree distribution with exponent $\gamma>3$ has been investigated using different mean-field approaches, which predict different outcomes. We performed extensive simulations in the quasistationary state for a comparison with these mean-field theories. We observed concomitant multiple transitions in individual networks presenting large gaps in the degree distribution and the obtained multiple epidemic thresholds are well described by different mean-field theories. We observed that the transitions involving thresholds which vanishes at the thermodynamic limit involve localized states, in which a vanishing fraction of the network effectively contribute to epidemic activity, whereas an endemic state, with a finite density of infected vertices, occurs at a finite threshold. The multiple transitions are related to the activations of distinct sub-domains of the network, which are not directly connected.Comment: This is a final version that will appear soon in Phys. Rev.

Activation thresholds in epidemic spreading with motile infectious agents on scale-free networks

We investigate a fermionic susceptible-infected-susceptible model with mobility of infected individuals on uncorrelated scale-free networks with power-law degree distributions $P (k) \sim k^{-\gamma}$ of exponents $2<\gamma<3$. Two diffusive processes with diffusion rate $D$ of an infected vertex are considered. In the \textit{standard diffusion}, one of the nearest-neighbors is chosen with equal chance while in the \textit{biased diffusion} this choice happens with probability proportional to the neighbor's degree. A non-monotonic dependence of the epidemic threshold on $D$ with an optimum diffusion rate $D_\ast$, for which the epidemic spreading is more efficient, is found for standard diffusion while monotonic decays are observed in the biased case. The epidemic thresholds go to zero as the network size is increased and the form that this happens depends on the diffusion rule and degree exponent. We analytically investigated the dynamics using quenched and heterogeneous mean-field theories. The former presents, in general, a better performance for standard and the latter for biased diffusion models, indicating different activation mechanisms of the epidemic phases that are rationalized in terms of hubs or max $k$-core subgraphs.Comment: 9 pages, 4 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

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