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We investigate the effects of modular and temporal connectivity patterns on epidemic spreading. To this end, we introduce and analytically characterise a model of time-varying networks with tunable modularity. Within this framework, we study the epidemic size of Susceptible-Infected-Recovered, SIR, models and the epidemic threshold of Susceptible-Infected-Susceptible, SIS, models. Interestingly, we find that while the presence of tightly connected clusters inhibit SIR processes, it speeds up SIS diseases. In this case, we observe that heterogeneous temporal connectivity patterns and modular structures induce a reduction of the threshold with respect to time-varying networks without communities. We confirm the theoretical results by means of extensive numerical simulations both on synthetic graphs as well as on a real modular and temporal network.
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Social interactions are stratified in multiple contexts and are subject to complex temporal dynamics. The systematic study of these two features of social systems has started only very recently mainly thanks to the development of multiplex and time-varying networks. However, these two advancements have progressed almost in parallel with very little overlap. Thus, the interplay between multiplexity and the temporal nature of connectivity patterns is poorly understood. Here, we aim to tackle this limitation by introducing a time-varying model of multiplex networks. We are interested in characterizing how these two properties affect contagion processes. To this end, we study SIS epidemic models unfolding at comparable time-scale respect to the evolution of the multiplex network. We study both analytically and numerically the epidemic threshold as a function of the overlap between, and the features of, each layer. We found that, the overlap between layers significantly reduces the epidemic threshold especially when the temporal activation patterns of overlapping nodes are positively correlated. Furthermore, when the average connectivity across layers is very different, the contagion dynamics are driven by the features of the more densely connected layer. Here, the epidemic threshold is equivalent to that of a single layered graph and the impact of the disease, in the layer driving the contagion, is independent of the overlap. However, this is not the case in the other layers where the spreading dynamics are sharply influenced by it. The results presented provide another step towards the characterization of the properties of real networks and their effects on contagion phenomena
A model for epidemic spreading on rewiring networks is introduced and analyzed for the case of scale free steady state networks. It is found that contrary to what one would have naively expected, the rewiring process typically tends to suppress epidemic spreading. In particular it is found that as in static networks, rewiring networks with degree distribution exponent $gamma >3$ exhibit a threshold in the infection rate below which epidemics die out in the steady state. However the threshold is higher in the rewiring case. For $2<gamma leq 3$ no such threshold exists, but for small infection rate the steady state density of infected nodes (prevalence) is smaller for rewiring networks.
In the past few decades, the frequency of pandemics has been increased due to the growth of urbanization and mobility among countries. Since a disease spreading in one country could become a pandemic with a potential worldwide humanitarian and economic impact, it is important to develop models to estimate the probability of a worldwide pandemic. In this paper, we propose a model of disease spreading in a structural modular complex network (having communities) and study how the number of bridge nodes $n$ that connect communities affects disease spread. We find that our model can be described at a global scale as an infectious transmission process between communities with global infectious and recovery time distributions that depend on the internal structure of each community and $n$. We find that near the critical point as $n$ increases, the disease reaches most of the communities, but each community has only a small fraction of recovered nodes. In addition, we obtain that in the limit $n to infty$, the probability of a pandemic increases abruptly at the critical point. This scenario could make the decision on whether to launch a pandemic alert or not more difficult. Finally, we show that link percolation theory can be used at a global scale to estimate the probability of a pandemic since the global transmissibility between communities has a weak dependence on the global recovery time.
Epidemic spread on networks is one of the most studied dynamics in network science and has important implications in real epidemic scenarios. Nonetheless, the dynamics of real epidemics and how it is affected by the underline structure of the infection channels are still not fully understood. Here we apply the SIR model and study analytically and numerically the epidemic spread on a recently developed spatial modular model imitating the structure of cities in a country. The model assumes that inside a city the infection channels connect many different locations, while the infection channels between cities are less and usually directly connect only a few nearest neighbor cities in a two-dimensional plane. We find that the model experience two epidemic transitions. The first lower threshold represents a local epidemic spread within a city but not to the entire country and the second higher threshold represents a global epidemic in the entire country. Based on our analytical solution we proposed several control strategies and how to optimize them. We also show that while control strategies can successfully control the disease, early actions are essentials to prevent the disease global spread.
We investigate the effect of degree correlation on a susceptible-infected-susceptible (SIS) model with a nonlinear cooperative effect (synergy) in infectious transmissions. In a mean-field treatment of the synergistic SIS model on a bimodal network with tunable degree correlation, we identify a discontinuous transition that is independent of the degree correlation strength unless the synergy is absent or extremely weak. Regardless of synergy (absent or present), a positive and negative degree correlation in the model reduces and raises the epidemic threshold, respectively. For networks with a strongly positive degree correlation, the mean-field treatment predicts the emergence of two discontinuous jumps in the steady-state infected density. To test the mean-field treatment, we provide approximate master equations of the present model, which accurately describe the synergistic SIS dynamics. We quantitatively confirm all qualitative predictions of the mean-field treatment in numerical evaluations of the approximate master equations.
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