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Register a new userFeedback pinning control of collective behaviors aroused by epidemic spread on complex networks
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This paper investigates epidemic control behavioral synchronization for a class of complex networks resulting from spread of epidemic diseases via pinning feedback control strategy. Based on the quenched mean field theory, epidemic control synchronization models with inhibition of contact behavior is constructed, combining with the epidemic transmission system and the complex dynamical network carrying extra controllers. By the properties of convex functions and Gerschgorin theorem, the epidemic threshold of the model is obtained, and the global stability of disease-free equilibrium is analyzed. For individuals infected situation, when epidemic spreads, two types of feedback control strategies depended on the diseases information are designed: the one only adds controllers to infected individuals, the other adds controllers both to infected and susceptible ones. And by using Lyapunov stability theory, under designed controllers, some criteria that guarantee epidemic control synchronization system achieving behavior synchronization are also derived. Several numerical simulations are performed to show the effectiveness of our theoretical results. As far as we know, this is the first work to address the controlling behavioral synchronization induced by epidemic spreading under the pinning feedback mechanism. It is hopeful that we may have more deeper insight into the essence between diseases spreading and collective behavior controlling in complex dynamical networks.
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One of the popular dynamics on complex networks is the epidemic spreading. An epidemic model describes how infections spread throughout a network. Among the compartmental models used to describe epidemics, the Susceptible-Infected-Susceptible (SIS) model has been widely used. In the SIS model, each node can be susceptible, become infected with a given infection rate, and become again susceptible with a given curing rate. In this paper, we add a new compartment to the classic SIS model to account for human response to epidemic spread. Each individual can be infected, susceptible, or alert. Susceptible individuals can become alert with an alerting rate if infected individuals exist in their neighborhood. An individual in the alert state is less probable to become infected than an individual in the susceptible state; due to a newly adopted cautious behavior. The problem is formulated as a continuous-time Markov process on a general static graph and then modeled into a set of ordinary differential equations using mean field approximation method and the corresponding Kolmogorov forward equations. The model is then studied using results from algebraic graph theory and center manifold theorem. We analytically show that our model exhibits two distinct thresholds in the dynamics of epidemic spread. Below the first threshold, infection dies out exponentially. Beyond the second threshold, infection persists in the steady state. Between the two thresholds, the infection spreads at the first stage but then dies out asymptotically as the result of increased alertness in the network. Finally, simulations are provided to support our findings. Our results suggest that alertness can be considered as a strategy of controlling the epidemics which propose multiple potential areas of applications, from infectious diseases mitigations to malware impact reduction.
Real epidemic spreading networks often composed of several kinds of networks interconnected with each other, and the interrelated networks have the different topologies and epidemic dynamics. Moreover, most human diseases are derived from animals, and the zoonotic infections always spread on interconnected networks. In this paper, we consider the epidemic spreading on one-way circular-coupled network consist of three interconnected subnetworks. Here, two one-way three-layer circular interactive networks are established by introducing the heterogeneous mean-field approach method, then we get the basic reproduction numbers and prove the global stability of the disease-free equilibrium and endemic equilibrium of the models. Through mathematical analysis and numerical simulations, it is found that the basic reproduction numbers $R_0$ of the two models are dependent on the infection rates, infection periods, average degrees and degree ratios. In the first model, the network structures of the inner contact patterns have a bigger impact on $R_0$ than that of the cross contact patterns. Under the same contact pattern, the internal infection rates have greater influence on $R_0$ than the cross-infection rates. In the second model, the disease prevails in a heterogeneous network has a greater impact on $R_0$ than the disease from a homogeneous network, and the infections among the three subnetworks all play a important role in the propagation process. Numerical examples verify and expand these theoretical results very well.
In the real world, many complex systems interact with other systems. In addition, the intra- or inter-systems for the spread of information about infectious diseases and the transmission of infectious diseases are often not random, but with direction. Hence, in this paper, we build epidemic model based on an interconnected directed network, which can be considered as the generalization of undirected networks and bipartite networks. By using the mean-field approach, we establish the Susceptible-Infectious-Susceptible model on this network. We theoretically analyze the model, and obtain the basic reproduction number, which is also the generalization of the critical number corresponding to undirected or bipartite networks. And we prove the global stability of disease-free and endemic equilibria via the basic reproduction number as a forward bifurcation parameter. We also give a condition for epidemic prevalence only on a single subnetwork. Furthermore, we carry out numerical simulations, and find that the independence between each nodes in- and out-degrees greatly reduce the impact of the networks topological structure on disease spread.
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.
Much recent empirical evidence shows that textit{community structure} is ubiquitous in the real-world networks. In this Letter, we propose a growth model to create scale-free networks with the tunable strength (noted by $Q$) of community structure and investigate the influence of community strength upon the collective synchronization induced by SIRS epidemiological process. Global and local synchronizability of the system is studied by means of an order parameter and the relevant finite-size scaling analysis is provided. The numerical results show that, a phase transition occurs at $Q_csimeq0.835$ from global synchronization to desynchronization and the local synchronization is weakened in a range of intermediately large $Q$. Moreover, we study the impact of mean degree $<k>$ upon synchronization on scale-free networks.
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