Modeling the Spread of Multiple Contagions on Multilayer Networks (original) (raw)
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System Dynamics of a Refined Epidemic Model for Infection Propagation Over Complex Networks
IEEE Systems Journal, 2014
The ability to predict future epidemic threats, both in real and digital worlds, and to develop effective containment strategies heavily leans on the availability of reliable infection spreading models. The stochastic behavior of such processes makes them even more demanding to scrutinize over structured networks. This paper concerns the dynamics of a new susceptible–infected–susceptible (SIS) epidemic model incorporated with multistage infection (infection delay) and an infective medium (propagation vector) over complex networks. In particular, we investigate the critical epidemic thresholds and the infection spreading pattern using mean-field approximation (MFA) and results obtained through extensive numerical simulations. We further generalize the model for any arbitrary number of infective media to mimic existing scenarios in biological and social networks. Our analysis and simulation results reveal that the inclusion of multiple infective medium and multiple stages of infection significantly alleviates the epidemic threshold and, thus, accelerates the process of infection spreading in the population.
Different epidemic models on complex networks
2009
Models for diseases spreading are not just limited to SIS or SIR. For instance, for the spreading of AIDS/HIV, the susceptible individuals can be classified into different cases according to their immunity, and similarly, the infected individuals can be sorted into different classes according to their infectivity. Moreover, some diseases may develop through several stages. Many authors have shown that the individuals' relation can be viewed as a complex network. So in this paper, in order to better explain the dynamical behavior of epidemics, we consider different epidemic models on complex networks, and obtain the epidemic threshold for each case. Finally, we present numerical simulations for each case to verify our results.
Competitive epidemic spreading over arbitrary multilayer networks
Physical Review E, 2014
This study extends the Susceptible-Infected-Susceptible (SIS) epidemic model for single-virus propagation over an arbitrary graph to an Susceptible-Infected by virus 1-Susceptible-Infected by virus 2-Susceptible (SI 1 SI 2 S) epidemic model of two exclusive, competitive viruses over a two-layer network with generic structure, where network layers represent the distinct transmission routes of the viruses. We find analytical expressions determining extinction, coexistence, and absolute dominance of the viruses after we introduce the concepts of survival threshold and absolute-dominance threshold. The main outcome of our analysis is the discovery and proof of a region for long-term coexistence of competitive viruses in nontrivial multilayer networks. We show coexistence is impossible if network layers are identical yet possible if network layers are distinct. Not only do we rigorously prove a region of coexistence, but we can quantitate it via interrelation of central nodes across the network layers. Little to no overlapping of the layers' central nodes is the key determinant of coexistence. For example, we show both analytically and numerically that positive correlation of network layers makes it difficult for a virus to survive, while in a network with negatively correlated layers, survival is easier, but total removal of the other virus is more difficult.
Susceptible-infected-susceptible epidemics on networks with general infection and cure times
Physical Review E, 2013
The classical, continuous-time susceptible-infected-susceptible (SIS) Markov epidemic model on an arbitrary network is extended to incorporate infection and curing or recovery times each characterized by a general distribution (rather than an exponential distribution as in Markov processes). This extension, called the generalized SIS (GSIS) model, is believed to have a much larger applicability to real-world epidemics (such as information spread in online social networks, real diseases, malware spread in computer networks, etc.) that likely do not feature exponential times. While the exact governing equations for the GSIS model are difficult to deduce due to their non-Markovian nature, accurate mean-field equations are derived that resemble our previous Nintertwined mean-field approximation (NIMFA) and so allow us to transfer the whole analytic machinery of the NIMFA to the GSIS model. In particular, we establish the criterion to compute the epidemic threshold in the GSIS model. Moreover, we show that the average number of infection attempts during a recovery time is the more natural key parameter, instead of the effective infection rate in the classical, continuous-time SIS Markov model. The relative simplicity of our mean-field results enables us to treat more general types of SIS epidemics, while offering an easier key parameter to measure the average activity of those general viral agents.
The Effects of Diffusion of Information on Epidemic Spread --- A Multilayer Approach
Acta Physica Polonica B
In this work, the aim is to study the spread of a contagious disease and information on a multilayer social system. The main idea is to find a criterion under which the adoption of the spreading information blocks or suppresses the epidemic spread. A two-layer network is the base of the model. The first layer describes the direct contact interactions, while the second layer is the information propagation layer. Both layers consist of the same nodes. The society consists of five different categories of individuals: susceptibles, infective, recovered, vaccinated and precautioned. Initially, only one infected individual starts transmitting the infection. Direct contact interactions spread the infection to the susceptibles. The information spreads through the second layer. The SIR model is employed for the infection spread, while the Bass equation models the adoption of information. The control parameters of the competition between the spread of information and spread of disease are the topology and the density of connectivity. The topology of the information layer is a scale-free network with increasing density of edges. In the contact layer, regular and scale-free networks with the same average degree per node are used interchangeably. The observation is that increasing complexity of the contact network reduces the role of individual awareness. If the contact layer consists of networks with limited range connections, or the edges sparser than the information network, spread of information plays a significant role in controlling the epidemics.
Epidemic Model with Isolation in Multilayer Networks
Scientific Reports, 2015
The Susceptible-Infected-Recovered (SIR) model has successfully mimicked the propagation of such airborne diseases as influenza A (H1N1). Although the SIR model has recently been studied in a multilayer networks configuration, in almost all the research the dynamic movement of infected individuals, e.g., how they are often kept in isolation, is disregarded. We study the SIR model in two multilayer networks and use an isolation parameter-indicating time period-to measure the effect of isolating infected individuals from both layers. This isolation reduces the transmission of the disease because the time in which infection can spread is reduced.
Time Evolution of Disease Spread on Networks with Degree Heterogeneity
2007
Two crucial elements facilitate the understanding and control of communicable disease spread within a social setting. These components are, the underlying contact structure among individuals that determines the pattern of disease transmission; and the evolution of this pattern over time. Mathematical models of infectious diseases, which are in principle analytically tractable, use two general approaches to incorporate these elements. The first approach, generally known as compartmental modeling, addresses the time evolution of disease spread at the expense of simplifying the pattern of transmission. On the other hand, the second approach uses network theory to incorporate detailed information pertaining to the underlying contact structure among individuals. However, while providing accurate estimates on the final size of outbreaks/epidemics, this approach, in its current formalism, disregards the progression of time during outbreaks. So far, the only alternative that enables the int...
Physical Review E, 2012
Recent work has shown that different theoretical approaches to the dynamics of the susceptible-infectedsusceptible (SIS) model for epidemics lead to qualitatively different estimates for the position of the epidemic threshold in networks. Here we present large-scale numerical simulations of the SIS dynamics on various types of networks, allowing the precise determination of the effective threshold for systems of finite size N . We compare quantitatively the numerical thresholds with theoretical predictions of the heterogeneous mean-field theory and of the quenched mean-field theory. We show that the latter is in general more accurate, scaling with N with the correct exponent, but often failing to capture the correct prefactor.
Network-based models of transmission of infectious diseases: a brief overview
2015
The main purpose of this document is to give a brief but mathematically rigorous description of the network-based models of transmission of infectious diseases that are studied on this web site1. Readers will be able to find a much more detailed development of this material in our book chapters [5, 6]. We also briefly describe how the network-based models that are defined here are related to compartment-level models that are used in most on the literature on mathematical epidemiology.
Epidemic spread in human networks
IEEE Conference on Decision and Control and European Control Conference, 2011
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.