The Behavior of Epidemics under Bounded Susceptibility

We investigate the sensitivity of epidemic behavior to a bounded susceptibility constraint -- susceptible nodes are infected by their neighbors via the regular SI/SIS dynamics, but subject to a cap on the infection rate. Such a constraint is motivated by modern social networks, wherein messages are broadcast to all neighbors, but attention spans are limited. Bounded susceptibility also arises in distributed computing applications with download bandwidth constraints, and in human epidemics under quarantine policies. Network epidemics have been extensively studied in literature; prior work characterizes the graph structures required to ensure fast spreading under the SI dynamics, and long lifetime under the SIS dynamics. In particular, these conditions turn out to be meaningful for two classes of networks of practical relevance -- dense, uniform (i.e., clique-like) graphs, and sparse, structured (i.e., star-like) graphs. We show that bounded susceptibility has a surprising impact on epidemic behavior in these graph families. For the SI dynamics, bounded susceptibility has no effect on star-like networks, but dramatically alters the spreading time in clique-like networks. In contrast, for the SIS dynamics, clique-like networks are unaffected, but star-like networks exhibit a sharp change in extinction times under bounded susceptibility. Our findings are useful for the design of disease-resistant networks and infrastructure networks. More generally, they show that results for existing epidemic models are sensitive to modeling assumptions in non-intuitive ways, and suggest caution in directly using these as guidelines for real systems

Network Inoculation: Heteroclinics and phase transitions in an epidemic model

In epidemiological modelling, dynamics on networks, and in particular adaptive and heterogeneous networks have recently received much interest. Here we present a detailed analysis of a previously proposed model that combines heterogeneity in the individuals with adaptive rewiring of the network structure in response to a disease. We show that in this model qualitative changes in the dynamics occur in two phase transitions. In a macroscopic description one of these corresponds to a local bifurcation whereas the other one corresponds to a non-local heteroclinic bifurcation. This model thus provides a rare example of a system where a phase transition is caused by a non-local bifurcation, while both micro- and macro-level dynamics are accessible to mathematical analysis. The bifurcation points mark the onset of a behaviour that we call network inoculation. In the respective parameter region exposure of the system to a pathogen will lead to an outbreak that collapses, but leaves the network in a configuration where the disease cannot reinvade, despite every agent returning to the susceptible class. We argue that this behaviour and the associated phase transitions can be expected to occur in a wide class of models of sufficient complexity.Comment: 26 pages, 11 figure

Epidemics on random intersection graphs

In this paper we consider a model for the spread of a stochastic SIR (Susceptible $\to$ Infectious $\to$ Recovered) epidemic on a network of individuals described by a random intersection graph. Individuals belong to a random number of cliques, each of random size, and infection can be transmitted between two individuals if and only if there is a clique they both belong to. Both the clique sizes and the number of cliques an individual belongs to follow mixed Poisson distributions. An infinite-type branching process approximation (with type being given by the length of an individual's infectious period) for the early stages of an epidemic is developed and made fully rigorous by proving an associated limit theorem as the population size tends to infinity. This leads to a threshold parameter $R_*$, so that in a large population an epidemic with few initial infectives can give rise to a large outbreak if and only if $R_*>1$. A functional equation for the survival probability of the approximating infinite-type branching process is determined; if $R_*\le1$, this equation has no nonzero solution, while if $R_*>1$, it is shown to have precisely one nonzero solution. A law of large numbers for the size of such a large outbreak is proved by exploiting a single-type branching process that approximates the size of the susceptibility set of a typical individual.Comment: Published in at http://dx.doi.org/10.1214/13-AAP942 the Annals of Applied Probability (http://www.imstat.org/aap/) by the Institute of Mathematical Statistics (http://www.imstat.org

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

Optimized Gillespie algorithms for the simulation of Markovian epidemic processes on large and heterogeneous networks

Numerical simulation of continuous-time Markovian processes is an essential and widely applied tool in the investigation of epidemic spreading on complex networks. Due to the high heterogeneity of the connectivity structure through which epidemics is transmitted, efficient and accurate implementations of generic epidemic processes are not trivial and deviations from statistically exact prescriptions can lead to uncontrolled biases. Based on the Gillespie algorithm (GA), in which only steps that change the state are considered, we develop numerical recipes and describe their computer implementations for statistically exact and computationally efficient simulations of generic Markovian epidemic processes aiming at highly heterogeneous and large networks. The central point of the recipes investigated here is to include phantom processes, that do not change the states but do count for time increments. We compare the efficiencies for the susceptible-infected-susceptible, contact process and susceptible-infected-recovered models, that are particular cases of a generic model considered here. We numerically confirm that the simulation outcomes of the optimized algorithms are statistically indistinguishable from the original GA and can be several orders of magnitude more efficient.Comment: 12 pages, 9 figure