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Register a new userWinning the competition: enhancing counter-contagion in SIS-like epidemic processes
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Added by
Argyris Kalogeratos
Publication date
2020
fields
Informatics Engineering
and research's language is
English
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In this paper we consider the epidemic competition between two generic diffusion processes, where each competing side is represented by a different state of a stochastic process. For this setting, we present the Generalized Largest Reduction in Infectious Edges (gLRIE) dynamic resource allocation strategy to advantage the preferred state against the other. Motivated by social epidemics, we apply this method to a generic continuous-time SIS-like diffusion model where we allow for: i) arbitrary node transition rate functions that describe the dynamics of propagation depending on the network state, and ii) competition between the healthy (positive) and infected (negative) states, which are both diffusive at the same time, yet mutually exclusive on each node. Finally we use simulations to compare empirically the proposed gLRIE against competitive approaches from literature.
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In this paper, we analyze dynamic switching networks, wherein the networks switch arbitrarily among a set of topologies. For this class of dynamic networks, we derive an epidemic threshold, considering the SIS epidemic model. First, an epidemic probabilistic model is developed assuming independence between states of nodes. We identify the conditions under which the epidemic dies out by linearizing the underlying dynamical system and analyzing its asymptotic stability around the origin. The concept of joint spectral radius is then used to derive the epidemic threshold, which is later validated using several networks (Watts-Strogatz, Barabasi-Albert, MIT reality mining graphs, Regular, and Gilbert). A simplified version of the epidemic threshold is proposed for undirected networks. Moreover, in the case of static networks, the derived epidemic threshold is shown to match conventional analytical results. Then, analytical results for the epidemic threshold of dynamic networksare proved to be applicable to periodic networks. For dynamic regular networks, we demonstrate that the epidemic threshold is identical to the epidemic threshold for static regular networks. An upper bound for the epidemic spread probability in dynamic Gilbert networks is also derived and verified using simulation.
The contagion dynamics can emerge in social networks when repeated activation is allowed. An interesting example of this phenomenon is retweet cascades where users allow to re-share content posted by other people with public accounts. To model this type of behaviour we use a Hawkes self-exciting process. To do it properly though one needs to calibrate model under consideration. The main goal of this paper is to construct moments method of estimation of this model. The key step is based on identifying of a generator of a Hawkes process. We perform numerical analysis on real data as well.
Networks are landmarks of many complex phenomena where interweaving interactions between different agents transform simple local rule-sets into nonlinear emergent behaviors. While some recent studies unveil associations between the network structure and the underlying dynamical process, identifying stochastic nonlinear dynamical processes continues to be an outstanding problem. Here we develop a simple data-driven framework based on operator-theoretic techniques to identify and control stochastic nonlinear dynamics taking place over large-scale networks. The proposed approach requires no prior knowledge of the network structure and identifies the underlying dynamics solely using a collection of two-step snapshots of the states. This data-driven system identification is achieved by using the Koopman operator to find a low dimensional representation of the dynamical patterns that evolve linearly. Further, we use the global linear Koopman model to solve critical control problems by applying to model predictive control (MPC)--typically, a challenging proposition when applied to large networks. We show that our proposed approach tackles this by converting the original nonlinear programming into a more tractable optimization problem that is both convex and with far fewer variables.
We propose a mathematical model to study coupled epidemic and opinion dynamics in a network of communities. Our model captures SIS epidemic dynamics whose evolution is dependent on the opinions of the communities toward the epidemic, and vice versa. In particular, we allow both cooperative and antagonistic interactions, representing similar and opposing perspectives on the severity of the epidemic, respectively. We propose an Opinion-Dependent Reproduction Number to characterize the mutual influence between epidemic spreading and opinion dissemination over the networks. Through stability analysis of the equilibria, we explore the impact of opinions on both epidemic outbreak and eradication, characterized by bounds on the Opinion-Dependent Reproduction Number. We also show how to eradicate epidemics by reshaping the opinions, offering researchers an approach for designing control strategies to reach target audiences to ensure effective epidemic suppression.
Albeit epidemic models have evolved into powerful predictive tools for the spread of diseases and opinions, most assume memoryless agents and independent transmission channels. We develop an infection mechanism that is endowed with memory of past exposures and simultaneously incorporates the joint effect of multiple infectious sources. Analytic equations and simulations of the susceptible-infected-susceptible model in unstructured substrates reveal the emergence of an additional phase that separates the usual healthy and endemic ones. This intermediate phase shows fundamentally distinct characteristics, and the system exhibits either excitability or an exotic variant of bistability. Moreover, the transition to endemicity presents hybrid aspects. These features are the product of an intricate balance between two memory modes and indicate that non-Markovian effects significantly alter the properties of spreading processes.
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