Modeling the dynamical interaction between epidemics on overlay networks

Epidemics seldom occur as isolated phenomena. Typically, two or more viral agents spread within the same host population and may interact dynamically with each other. We present a general model where two viral agents interact via an immunity mechanism as they propagate simultaneously on two networks connecting the same set of nodes. Exploiting a correspondence between the propagation dynamics and a dynamical process performing progressive network generation, we develop an analytic approach that accurately captures the dynamical interaction between epidemics on overlay networks. The formalism allows for overlay networks with arbitrary joint degree distribution and overlap. To illustrate the versatility of our approach, we consider a hypothetical delayed intervention scenario in which an immunizing agent is disseminated in a host population to hinder the propagation of an undesirable agent (e.g. the spread of preventive information in the context of an emerging infectious disease).Comment: Accepted for publication in Phys. Rev. E. 15 pages, 7 figure

Coupled effects of local movement and global interaction on contagion

By incorporating segregated spatial domain and individual-based linkage into the SIS (susceptible-infected-susceptible) model, we investigate the coupled effects of random walk and intragroup interaction on contagion. Compared with the situation where only local movement or individual-based linkage exists, the coexistence of them leads to a wider spread of infectious disease. The roles of narrowing segregated spatial domain and reducing mobility in epidemic control are checked, these two measures are found to be conducive to curbing the spread of infectious disease. Considering heterogeneous time scales between local movement and global interaction, a log-log relation between the change in the number of infected individuals and the timescale $\tau$ is found. A theoretical analysis indicates that the evolutionary dynamics in the present model is related to the encounter probability and the encounter time. A functional relation between the epidemic threshold and the ratio of shortcuts, and a functional relation between the encounter time and the timescale $\tau$ are found

Epidemics in Networks of Spatially Correlated Three-dimensional Root Branching Structures

Using digitized images of the three-dimensional, branching structures for root systems of bean seedlings, together with analytical and numerical methods that map a common 'SIR' epidemiological model onto the bond percolation problem, we show how the spatially-correlated branching structures of plant roots affect transmission efficiencies, and hence the invasion criterion, for a soil-borne pathogen as it spreads through ensembles of morphologically complex hosts. We conclude that the inherent heterogeneities in transmissibilities arising from correlations in the degrees of overlap between neighbouring plants, render a population of root systems less susceptible to epidemic invasion than a corresponding homogeneous system. Several components of morphological complexity are analysed that contribute to disorder and heterogeneities in transmissibility of infection. Anisotropy in root shape is shown to increase resilience to epidemic invasion, while increasing the degree of branching enhances the spread of epidemics in the population of roots. Some extension of the methods for other epidemiological systems are discussed.Comment: 21 pages, 8 figure

Understanding HIV/AIDS in the African Context

This book of readings is intended for courses in Global Health. The editors asked Prof. Stillwaggon to contribute a chapter summarizing her years of work on the spread of HIV/AIDS in populations among whom bacterial, fungal, parasitic, and viral diseases are extremely common, particularly in sub-Saharan Africa. Her work has demonstrated that differences in behavior cannot explain differences in HIV rates between world regions

Epidemic model with isolation in multilayer networks

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 isolation of infected individuals is disregarded. Hence we focus our study in an epidemic model in a two-layer network and we use an isolation parameter w to measure the effect of quarantining infected individuals from both layers during an isolation period tw. We call this process the Susceptible-Infected-Isolated-Recovered (SIIR) model. Using the framework of link percolation we find that isolation increases the critical epidemic threshold of the disease because the time in which infection can spread is reduced. In this scenario we find that this threshold increases with w and tw. When the isolation period is maximum there is a critical threshold for w above which the disease never becomes an epidemic. We simulate the process and find an excellent agreement with the theoretical results.We thank the NSF (grants CMMI 1125290 and CHE-1213217) and the Keck Foundation for financial support. LGAZ and LAB wish to thank to UNMdP and FONCyT (Pict 0429/2013) for financial support. (CMMI 1125290 - NSF; CHE-1213217 - NSF; Keck Foundation; UNMdP; Pict 0429/2013 - FONCyT)Published versio

Epidemic Model with Isolation in Multilayer Networks

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 isolation of infected individuals is disregarded. Hence we focus our study in an epidemic model in a two-layer network, and we use an isolation parameter to measure the effect of isolating infected individuals from both layers during an isolation period. We call this process the Susceptible-Infected-Isolated-Recovered ($SI_IR$) model. The isolation reduces the transmission of the disease because the time in which infection can spread is reduced. In this scenario we find that the epidemic threshold increases with the isolation period and the isolation parameter. When the isolation period is maximum there is a threshold for the isolation parameter above which the disease never becomes an epidemic. We also find that epidemic models, like $SIR$ overestimate the theoretical risk of infection. Finally, our model may provide a foundation for future research to study the temporal evolution of the disease calibrating our model with real data.Comment: 18 pages, 5 figures.Accepted in Scientific Report

Characterising two-pathogen competition in spatially structured environments

Different pathogens spreading in the same host population often generate complex co-circulation dynamics because of the many possible interactions between the pathogens and the host immune system, the host life cycle, and the space structure of the population. Here we focus on the competition between two acute infections and we address the role of host mobility and cross-immunity in shaping possible dominance/co-dominance regimes. Host mobility is modelled as a network of traveling flows connecting nodes of a metapopulation, and the two-pathogen dynamics is simulated with a stochastic mechanistic approach. Results depict a complex scenario where, according to the relation among the epidemiological parameters of the two pathogens, mobility can either be non-influential for the competition dynamics or play a critical role in selecting the dominant pathogen. The characterisation of the parameter space can be explained in terms of the trade-off between pathogen's spreading velocity and its ability to diffuse in a sparse environment. Variations in the cross-immunity level induce a transition between presence and absence of competition. The present study disentangles the role of the relevant biological and ecological factors in the competition dynamics, and provides relevant insights into the spatial ecology of infectious diseases.Comment: 30 pages, 6 figures, 1 table. Final version accepted for publication in Scientific Report

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