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Epidemic threshold is one of the most important features of the epidemic dynamics. Through a lot of numerical simulations in classic Susceptible-Infected-Recovered (SIR) and Susceptible-Infected-Susceptible (SIS) models on various types of networks, we study the simulated identification of epidemic thresholds on finite-size networks. We confirm that the susceptibility measure goes awry for the SIR model due to the bimodal distribution of outbreak sizes near the critical point, while the simulated thresholds of the SIS and SIR models can be accurately determined by analyzing the peak of the epidemic variability. We further verify the accuracy of theoretical predictions derived by the heterogeneous mean-field theory (HMF) and the quenched mean-field theory (QMF), by comparing them with the simulated threshold of the SIR model obtained from the variability measure. The results show that the HMF prediction agrees very well with the simulated threshold, except the case that the networks are disassortive, in which the QMF prediction is more close to the simulated threshold.
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The study of complex networks sheds light on the relation between the structure and function of complex systems. One remarkable result is the absence of an epidemic threshold in infinite-size scale-free networks, which implies that any infection will perpetually propagate regardless of the spreading rate. The vast majority of current theoretical approaches assumes that infections are transmitted as a reaction process from nodes to all neighbors. Here we adopt a different perspective and show that the epidemic incidence is shaped by traffic flow conditions. Specifically, we consider the scenario in which epidemic pathways are defined and driven by flows. Through extensive numerical simulations and theoretical predictions, it is shown that the value of the epidemic threshold in scale-free networks depends directly on flow conditions, in particular on the first and second moments of the betweenness distribution given a routing protocol. We consider the scenarios in which the delivery capability of the nodes is bounded or unbounded. In both cases, the threshold values depend on the traffic and decrease as flow increases. Bounded delivery provokes the emergence of congestion, slowing down the spreading of the disease and setting a limit for the epidemic incidence. Our results provide a general conceptual framework to understand spreading processes on complex networks.
We study the effect of heterogeneous temporal activations on epidemic spreading in temporal networks. We focus on the susceptible-infected-susceptible (SIS) model on activity-driven networks with burstiness. By using an activity-based mean-field approach, we derive a closed analytical form for the epidemic threshold for arbitrary activity and inter-event time distributions. We show that, as expected, burstiness lowers the epidemic threshold while its effect on prevalence is twofold. In low-infective systems burstiness raises the average infection probability, while it weakens epidemic spreading for high infectivity. Our results can help clarify the conflicting effects of burstiness reported in the literature. We also discuss the scaling properties at the transition, showing that they are not affected by burstiness.
In epidemic modeling, the term infection strength indicates the ratio of infection rate and cure rate. If the infection strength is higher than a certain threshold -- which we define as the epidemic threshold - then the epidemic spreads through the population and persists in the long run. For a single generic graph representing the contact network of the population under consideration, the epidemic threshold turns out to be equal to the inverse of the spectral radius of the contact graph. However, in a real world scenario it is not possible to isolate a population completely: there is always some interconnection with another network, which partially overlaps with the contact network. Results for epidemic threshold in interconnected networks are limited to homogeneous mixing populations and degree distribution arguments. In this paper, we adopt a spectral approach. We show how the epidemic threshold in a given network changes as a result of being coupled with another network with fixed infection strength. In our model, the contact network and the interconnections are generic. Using bifurcation theory and algebraic graph theory, we rigorously derive the epidemic threshold in interconnected networks. These results have implications for the broad field of epidemic modeling and control. Our analytical results are supported by numerical simulations.
Vaccination is an important measure available for preventing or reducing the spread of infectious diseases. In this paper, an epidemic model including susceptible, infected, and imperfectly vaccinated compartments is studied on Watts-Strogatz small-world, Barabasi-Albert scale-free, and random scale-free networks. The epidemic threshold and prevalence are analyzed. For small-world networks, the effective vaccination intervention is suggested and its influence on the threshold and prevalence is analyzed. For scale-free networks, the threshold is found to be strongly dependent both on the effective vaccination rate and on the connectivity distribution. Moreover, so long as vaccination is effective, it can linearly decrease the epidemic prevalence in small-world networks, whereas for scale-free networks it acts exponentially. These results can help in adopting pragmatic treatment upon diseases in structured populations.
can evolve simultaneously. For the information-driven adaptive process, susceptible (infected) individuals who have abilities to recognize the disease would break the links of their infected (susceptible) neighbors to prevent the epidemic from further spreading. Simulation results and numerical analyses based on the pairwise approach indicate that the information-driven adaptive process can not only slow down the speed of epidemic spreading, but can also diminish the epidemic prevalence at the final state significantly. In addition, the disease spreading and information diffusion pattern on the lattice give a visual representation about how the disease is trapped into an isolated field with the information-driven adaptive process. Furthermore, we perform the local bifurcation analysis on four types of dynamical regions, including healthy, oscillatory, bistable and endemic, to understand the evolution of the observed dynamical behaviors. This work may shed some lights on understanding how information affects human activities on responding to epidemic spreading.
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