Competing epidemics on complex networks

Human diseases spread over networks of contacts between individuals and a substantial body of recent research has focused on the dynamics of the spreading process. Here we examine a model of two competing diseases spreading over the same network at the same time, where infection with either disease gives an individual subsequent immunity to both. Using a combination of analytic and numerical methods, we derive the phase diagram of the system and estimates of the expected final numbers of individuals infected with each disease. The system shows an unusual dynamical transition between dominance of one disease and dominance of the other as a function of their relative rates of growth. Close to this transition the final outcomes show strong dependence on stochastic fluctuations in the early stages of growth, dependence that decreases with increasing network size, but does so sufficiently slowly as still to be easily visible in systems with millions or billions of individuals. In most regions of the phase diagram we find that one disease eventually dominates while the other reaches only a vanishing fraction of the network, but the system also displays a significant coexistence regime in which both diseases reach epidemic proportions and infect an extensive fraction of the network.Comment: 14 pages, 5 figure

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

Dynamics of new strain emergence on a temporal network

Multi-strain competition on networks is observed in many contexts, including infectious disease ecology, information dissemination or behavioral adaptation to epidemics. Despite a substantial body of research has been developed considering static, time-aggregated networks, it remains a challenge to understand the transmission of concurrent strains when links of the network are created and destroyed over time. Here we analyze how network dynamics shapes the outcome of the competition between an initially endemic strain and an emerging one, when both strains follow a susceptible-infected-susceptible dynamics, and spread at time scales comparable with the network evolution one. Using time-resolved data of close-proximity interactions between patients admitted to a hospital and medical health care workers, we analyze the impact of temporal patterns and initial conditions on the dominance diagram and coexistence time. We find that strong variations in activity volume cause the probability that the emerging strain replaces the endemic one to be highly sensitive to the time of emergence. The temporal structure of the network shapes the dominance diagram, with significant variations in the replacement probability (for a given set of epidemiological parameters) observed from the empirical network and a randomized version of it. Our work contributes towards the description of the complex interplay between competing pathogens on temporal networks.Comment: 9 pages, 4 figure

Spreading processes in Multilayer Networks

Several systems can be modeled as sets of interconnected networks or networks with multiple types of connections, here generally called multilayer networks. Spreading processes such as information propagation among users of an online social networks, or the diffusion of pathogens among individuals through their contact network, are fundamental phenomena occurring in these networks. However, while information diffusion in single networks has received considerable attention from various disciplines for over a decade, spreading processes in multilayer networks is still a young research area presenting many challenging research issues. In this paper we review the main models, results and applications of multilayer spreading processes and discuss some promising research directions.Comment: 21 pages, 3 figures, 4 table

Targeted Recovery as an Effective Strategy against Epidemic Spreading

We propose a targeted intervention protocol where recovery is restricted to individuals that have the least number of infected neighbours. Our recovery strategy is highly efficient on any kind of network, since epidemic outbreaks are minimal when compared to the baseline scenario of spontaneous recovery. In the case of spatially embedded networks, we find that an epidemic stays strongly spatially confined with a characteristic length scale undergoing a random walk. We demonstrate numerically and analytically that this dynamics leads to an epidemic spot with a flat surface structure and a radius that grows linearly with the spreading rate.Comment: 6 pages, 5 figure

Multi-state epidemic processes on complex networks

Infectious diseases are practically represented by models with multiple states and complex transition rules corresponding to, for example, birth, death, infection, recovery, disease progression, and quarantine. In addition, networks underlying infection events are often much more complex than described by meanfield equations or regular lattices. In models with simple transition rules such as the SIS and SIR models, heterogeneous contact rates are known to decrease epidemic thresholds. We analyze steady states of various multi-state disease propagation models with heterogeneous contact rates. In many models, heterogeneity simply decreases epidemic thresholds. However, in models with competing pathogens and mutation, coexistence of different pathogens for small infection rates requires network-independent conditions in addition to heterogeneity in contact rates. Furthermore, models without spontaneous neighbor-independent state transitions, such as cyclically competing species, do not show heterogeneity effects.Comment: 7 figures, 1 tabl