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Register a new userCollective versus hub activation of epidemic phases on networks
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We consider a general criterion to discern the nature of the threshold in epidemic models on scale-free (SF) networks. Comparing the epidemic lifespan of the nodes with largest degrees with the infection time between them, we propose a general dual scenario, in which the epidemic transition is either ruled by a hub activation process, leading to a null threshold in the thermodynamic limit, or given by a collective activation process, corresponding to a standard phase transition with a finite threshold. We validate the proposed criterion applying it to different epidemic models, with waning immunity or heterogeneous infection rates in both synthetic and real SF networks. In particular, a waning immunity, irrespective of its strength, leads to collective activation with finite threshold in scale-free networks with large exponent, at odds with canonical theoretical approaches.
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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.
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.
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 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.
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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