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Register a new userAnalysis of an epidemic model with awareness decay on regular random networks
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The existence of a die-out threshold (different from the classic disease-invasion one) defining a region of slow extinction of an epidemic has been proved elsewhere for susceptible-aware-infectious-susceptible models without awareness decay, through bifurcation analysis. By means of an equivalent mean-field model defined on regular random networks, we interpret the dynamics of the system in this region and prove that the existence of bifurcation for this second epidemic threshold crucially depends on the absence of awareness decay. We show that the continuum of equilibria that characterizes the slow die-out dynamics collapses into a unique equilibrium when a constant rate of awareness decay is assumed, no matter how small, and that the resulting bifurcation from the disease-free equilibrium is equivalent to that of standard epidemic models. We illustrate these findings with continuous-time stochastic simulations on regular random networks with different degrees. Finally, the behaviour of solutions with and without decay in awareness is compared around the second epidemic threshold for a small rate of awareness decay.
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In the study of infectious diseases on networks, researchers calculate epidemic thresholds to help forecast whether a disease will eventually infect a large fraction of a population. Because network structure typically changes in time, which fundamentally influences the dynamics of spreading processes on them and in turn affects epidemic thresholds for disease propagation, it is important to examine epidemic thresholds in temporal networks. Most existing studies of epidemic thresholds in temporal networks have focused on models in discrete time, but most real-world networked systems evolve continuously in time. In our work, we encode the continuous time-dependence of networks into the evaluation of the epidemic threshold of a susceptible--infected--susceptible (SIS) process by studying an SIS model on tie-decay networks. We derive the epidemic-threshold condition of this model, and we perform numerical experiments to verify it. We also examine how different factors---the decay coefficients of the tie strengths in a network, the frequency of interactions between nodes, and the sparsity of the underlying social network in which interactions occur---lead to decreases or increases of the critical values of the threshold and hence contribute to facilitating or impeding the spread of a disease. We thereby demonstrate how the features of tie-decay networks alter the outcome of disease spread.
In social networks, interaction patterns typically change over time. We study opinion dynamics on tie-decay networks in which tie strength increases instantaneously when there is an interaction and decays exponentially between interactions. Specifically, we formulate continuous-time Laplacian dynamics and a discrete-time DeGroot model of opinion dynamics on these tie-decay networks, and we carry out numerical computations for the continuous-time Laplacian dynamics. We examine the speed of convergence by studying the spectral gaps of combinatorial Laplacian matrices of tie-decay networks. First, we compare the spectral gaps of the Laplacian matrices of tie-decay networks that we construct from empirical data with the spectral gaps for corresponding randomized and aggregate networks. We find that the spectral gaps for the empirical networks tend to be smaller than those for the randomized and aggregate networks. Second, we study the spectral gap as a function of the tie-decay rate and time. Intuitively, we expect small tie-decay rates to lead to fast convergence because the influence of each interaction between two nodes lasts longer for smaller decay rates. Moreover, as time progresses and more interactions occur, we expect eventual convergence. However, we demonstrate that the spectral gap need not decrease monotonically with respect to the decay rate or increase monotonically with respect to time. Our results highlight the importance of the interplay between the times that edges strengthen and decay in temporal networks.
Public health services are constantly searching for new ways to reduce the spread of infectious diseases, such as public vaccination of asymptomatic individuals, quarantine (isolation) and treatment of symptomatic individuals. Epidemic models have a long history of assisting in public health planning and policy making. In this paper, we introduce epidemic models including variable population size, degree-related imperfect vaccination and quarantine on scale-free networks. More specifically, the models are formulated both on the population with and without permanent natural immunity to infection, which corresponds respectively to the susceptible-vaccinated-infected-quarantined-recovered (SVIQR) model and the susceptible-vaccinated-infected-quarantined (SVIQS) model. We develop different mathematical methods and techniques to study the dynamics of two models, including the basic reproduction number, the global stability of disease-free and endemic equilibria. For the SVIQR model, we show that the system exhibits a forward bifurcation. Meanwhile, the disease-free and unique endemic equilibria are shown to be globally asymptotically stable by constructing suitable Lyapunov functions. For the SVIQS model, conditions ensuring the occurrence of multiple endemic equilibria are derived. Under certain conditions, this system cannot undergo a backward bifurcation. The global asymptotical stability of disease-free equilibrium, and the persistence of the disease are proved. The endemic equilibrium is shown to be globally attractive by using monotone iterative technique. Finally, stochastic network simulations yield quantitative agreement with the deterministic mean-field approach.
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