Predicting the epidemic threshold of the susceptible-infected-recovered model

Researchers have developed several theoretical methods for predicting epidemic thresholds, including the mean-field like (MFL) method, the quenched mean-field (QMF) method, and the dynamical message passing (DMP) method. When these methods are applied to predict epidemic threshold they often produce differing results and their relative levels of accuracy are still unknown. We systematically analyze these two issues---relationships among differing results and levels of accuracy---by studying the susceptible-infected-recovered (SIR) model on uncorrelated configuration networks and a group of 56 real-world networks. In uncorrelated configuration networks the MFL and DMP methods yield identical predictions that are larger and more accurate than the prediction generated by the QMF method. When compared to the 56 real-world networks, the epidemic threshold obtained by the DMP method is closer to the actual epidemic threshold because it incorporates full network topology information and some dynamical correlations. We find that in some scenarios---such as networks with positive degree-degree correlations, with an eigenvector localized on the high $k$-core nodes, or with a high level of clustering---the epidemic threshold predicted by the MFL method, which uses the degree distribution as the only input parameter, performs better than the other two methods. We also find that the performances of the three predictions are irregular versus modularity

Large epidemic thresholds emerge in heterogeneous networks of heterogeneous nodes

One of the famous results of network science states that networks with heterogeneous connectivity are more susceptible to epidemic spreading than their more homogeneous counterparts. In particular, in networks of identical nodes it has been shown that network heterogeneity, i.e. a broad degree distribution, can lower the epidemic threshold at which epidemics can invade the system. Network heterogeneity can thus allow diseases with lower transmission probabilities to persist and spread. However, it has been pointed out that networks in which the properties of nodes are intrinsically heterogeneous can be very resilient to disease spreading. Heterogeneity in structure can enhance or diminish the resilience of networks with heterogeneous nodes, depending on the correlations between the topological and intrinsic properties. Here, we consider a plausible scenario where people have intrinsic differences in susceptibility and adapt their social network structure to the presence of the disease. We show that the resilience of networks with heterogeneous connectivity can surpass those of networks with homogeneous connectivity. For epidemiology, this implies that network heterogeneity should not be studied in isolation, it is instead the heterogeneity of infection risk that determines the likelihood of outbreaks

Asymmetrically interacting spreading dynamics on complex layered networks

The spread of disease through a physical-contact network and the spread of information about the disease on a communication network are two intimately related dynamical processes. We investigate the asymmetrical interplay between the two types of spreading dynamics, each occurring on its own layer, by focusing on the two fundamental quantities underlying any spreading process: epidemic threshold and the final infection ratio. We find that an epidemic outbreak on the contact layer can induce an outbreak on the communication layer, and information spreading can effectively raise the epidemic threshold. When structural correlation exists between the two layers, the information threshold remains unchanged but the epidemic threshold can be enhanced, making the contact layer more resilient to epidemic outbreak. We develop a physical theory to understand the intricate interplay between the two types of spreading dynamics.Comment: 29 pages, 14 figure

Suppressing disease spreading by using information diffusion on multiplex networks

Although there is always an interplay between the dynamics of information diffusion and disease spreading, the empirical research on the systemic coevolution mechanisms connecting these two spreading dynamics is still lacking. Here we investigate the coevolution mechanisms and dynamics between information and disease spreading by utilizing real data and a proposed spreading model on multiplex network. Our empirical analysis finds asymmetrical interactions between the information and disease spreading dynamics. Our results obtained from both the theoretical framework and extensive stochastic numerical simulations suggest that an information outbreak can be triggered in a communication network by its own spreading dynamics or by a disease outbreak on a contact network, but that the disease threshold is not affected by information spreading. Our key finding is that there is an optimal information transmission rate that markedly suppresses the disease spreading. We find that the time evolution of the dynamics in the proposed model qualitatively agrees with the real-world spreading processes at the optimal information transmission rate.Comment: 11 pages, 8 figure