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Register a new userEfficient mitigation strategies for epidemics in rural regions
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Containing an epidemic at its origin is the most desirable mitigation. Epidemics have often originated in rural areas, with rural communities among the first affected. Disease dynamics in rural regions have received limited attention, and results of general studies cannot be directly applied since population densities and human mobility factors are very different in rural regions from those in cities. We create a network model of a rural community in Kansas, USA, by collecting data on the contact patterns and computing rates of contact among a sampled population. We model the impact of different mitigation strategies detecting closely connected groups of people and frequently visited locations. Within those groups and locations, we compare the effectiveness of random and targeted vaccinations using a Susceptible-Exposed-Infected-Recovered compartmental model on the contact network. Our simulations show that the targeted vaccinations of only 10% of the sampled population reduced the size of the epidemic by 34.5%. Additionally, if 10% of the population visiting one of the most popular locations is randomly vaccinated, the epidemic size is reduced by 19%. Our results suggest a new implementation of a highly effective strategy for targeted vaccinations through the use of popular locations in rural communities.
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A two-state epidemic model in networks with links mimicking two kinds of relationships between connected nodes is introduced. Links of weights w1 and w0 occur with probabilities p and 1-p, respectively. The fraction of infected nodes rho(p) shows a non-monotonic behavior, with rho drops with p for small p and increases for large p. For small to moderate w1/w0 ratios, rho(p) exhibits a minimum that signifies an optimal suppression. For large w1/w0 ratios, the suppression leads to an absorbing phase consisting only of healthy nodes within a range p_L =< p =< p_R, and an active phase with mixed infected and healthy nodes for p < p_L and p>p_R. A mean field theory that ignores spatial correlation is shown to give qualitative agreement and capture all the key features. A physical picture that emphasizes the intricate interplay between infections via w0 links and within clusters formed by nodes carrying the w1 links is presented. The absorbing state at large w1/w0 ratios results when the clusters are big enough to disrupt the spread via w0 links and yet small enough to avoid an epidemic within the clusters. A theory that uses the possible local environments of a node as variables is formulated. The theory gives results in good agreement with simulation results, thereby showing the necessity of including longer spatial correlations.
Defining an optimal protection strategy against viruses, spam propagation or any other kind of contamination process is an important feature for designing new networks and architectures. In this work, we consider decentralized optimal protection strategies when a virus is propagating over a network through a SIS epidemic process. We assume that each node in the network can fully protect itself from infection at a constant cost, or the node can use recovery software, once it is infected. We model our system using a game theoretic framework and find pure, mixed equilibria, and the Price of Anarchy (PoA) in several network topologies. Further, we propose both a decentralized algorithm and an iterative procedure to compute a pure equilibrium in the general case of a multiple communities network. Finally, we evaluate the algorithms and give numerical illustrations of all our results.
Pathogens can spread epidemically through populations. Beneficial contagions, such as viruses that enhance host survival or technological innovations that improve quality of life, also have the potential to spread epidemically. How do the dynamics of beneficial biological and social epidemics differ from those of detrimental epidemics? We investigate this question using three theoretical approaches. First, in the context of population genetics, we show that a horizontally-transmissible element that increases fitness, such as viral DNA, spreads superexponentially through a population, more quickly than a beneficial mutation. Second, in the context of behavioral epidemiology, we show that infections that cause increased connectivity lead to superexponential fixation in the population. Third, in the context of dynamic social networks, we find that preferences for increased global infection accelerate spread and produce superexponential fixation, but preferences for local assortativity halt epidemics by disconnecting the infected from the susceptible. We conclude that the dynamics of beneficial biological and social epidemics are characterized by the rapid spread of beneficial elements, which is facilitated in biological systems by horizontal transmission and in social systems by active spreading behavior of infected individuals.
To improve the accuracy of network-based SIS models we introduce and study a multilayer representation of a time-dependent network. In particular, we assume that individuals have their long-term (permanent) contacts that are always present, identifying in this way the first network layer. A second network layer also exists, where the same set of nodes can be connected by occasional links, created with a given probability. While links of the first layer are permanent, a link of the second layer is only activated with some probability and under the condition that the two nodes, connected by this link, are simultaneously participating to the temporary link. We develop a model for the SIS epidemic on this time-dependent network, analyze equilibrium and stability of the corresponding mean-field equations, and shed some light on the role of the temporal layer on the spreading process.
We study structural changes of adaptive networks in the co-evolutionary susceptible-infected-susceptible (SIS) network model along its phase transition. We clarify to what extent these changes can be used as early-warning signs for the transition at the critical infection rate $lambda_c$ at which the network collapses and the system disintegrates. We analyze the interplay between topology and node-state dynamics near criticality. Several network measures exhibit clear maxima or minima close to the critical threshold that could potentially serve as early-warning signs. These measures include the $SI$ link density, triplet densities, clustering, assortativity and the eigenvalue gap. For the $SI$ link density and triplet densities the maximum is found to originate from the co-existence of two power laws. Other network quantities, such as the degree, the branching ratio, or the harmonic mean distance, show scaling with a singularity at $lambda=0$ and not at $lambda_c$, which means that they are incapable of detecting the transition.
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