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Register a new userOn the numerical study of percolation and epidemic critical properties in networks
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The static properties of the fundamental model for epidemics of diseases allowing immunity (susceptible-infected-removed model) are known to be derivable by an exact mapping to bond percolation. Yet when performing numerical simulations of these dynamics in a network a number of subtleties must be taken into account in order to correctly estimate the transition point and the associated critical properties. We expose these subtleties and identify the different quantities which play the role of criticality detector in the two dynamics.
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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.
In the last two decades, network science has blossomed and influenced various fields, such as statistical physics, computer science, biology and sociology, from the perspective of the heterogeneous interaction patterns of components composing the complex systems. As a paradigm for random and semi-random connectivity, percolation model plays a key role in the development of network science and its applications. On the one hand, the concepts and analytical methods, such as the emergence of the giant cluster, the finite-size scaling, and the mean-field method, which are intimately related to the percolation theory, are employed to quantify and solve some core problems of networks. On the other hand, the insights into the percolation theory also facilitate the understanding of networked systems, such as robustness, epidemic spreading, vital node identification, and community detection. Meanwhile, network science also brings some new issues to the percolation theory itself, such as percolation of strong heterogeneous systems, topological transition of networks beyond pairwise interactions, and emergence of a giant cluster with mutual connections. So far, the percolation theory has already percolated into the researches of structure analysis and dynamic modeling in network science. Understanding the percolation theory should help the study of many fields in network science, including the still opening questions in the frontiers of networks, such as networks beyond pairwise interactions, temporal networks, and network of networks. The intention of this paper is to offer an overview of these applications, as well as the basic theory of percolation transition on network systems.
Weak ties play a significant role in the structures and the dynamics of community networks. Based on the susceptible-infected model in contact process, we study numerically how weak ties influence the predictability of epidemic dynamics. We first investigate the effects of different kinds of weak ties on the variabilities of both the arrival time and the prevalence of disease, and find that the bridgeness with small degree can enhance the predictability of epidemic spreading. Once weak ties are settled, compared with the variability of arrival time, the variability of prevalence displays a diametrically opposed changing trend with both the distance of the initial seed to the bridgeness and the degree of the initial seed. More specifically, the further distance and the larger degree of the initial seed can induce the better predictability of arrival time and the worse predictability of prevalence. Moreover, we discuss the effects of weak tie number on the epidemic variability. As community strength becomes very strong, which is caused by the decrease of weak tie number, the epidemic variability will change dramatically. Compared with the case of hub seed and random seed, the bridgenss seed can result in the worst predictability of arrival time and the best predictability of prevalence. These results show that the variability of arrival time always marks a complete reversal trend of that of prevalence, which implies it is impossible to predict epidemic spreading in the early stage of outbreaks accurately.
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.
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.
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