skip to main content


Title: Connectivity, reproduction number, and mobility interact to determine communities’ epidemiological superspreader potential in a metapopulation network
Disease epidemic outbreaks on human metapopulation networks are often driven by a small number of superspreader nodes, which are primarily responsible for spreading the disease throughout the network. Superspreader nodes typically are characterized either by their locations within the network, by their degree of connectivity and centrality, or by their habitat suitability for the disease, described by their reproduction number ( R ). Here we introduce a model that considers simultaneously the effects of network properties and R on superspreaders, as opposed to previous research which considered each factor separately. This type of model is applicable to diseases for which habitat suitability varies by climate or land cover, and for direct transmitted diseases for which population density and mitigation practices influences R . We present analytical models that quantify the superspreader capacity of a population node by two measures: probability-dependent superspreader capacity, the expected number of neighboring nodes to which the node in consideration will randomly spread the disease per epidemic generation, and time-dependent superspreader capacity, the rate at which the node spreads the disease to each of its neighbors. We validate our analytical models with a Monte Carlo analysis of repeated stochastic Susceptible-Infected-Recovered (SIR) simulations on randomly generated human population networks, and we use a random forest statistical model to relate superspreader risk to connectivity, R , centrality, clustering, and diffusion. We demonstrate that either degree of connectivity or R above a certain threshold are sufficient conditions for a node to have a moderate superspreader risk factor, but both are necessary for a node to have a high-risk factor. The statistical model presented in this article can be used to predict the location of superspreader events in future epidemics, and to predict the effectiveness of mitigation strategies that seek to reduce the value of R , alter host movements, or both.  more » « less
Award ID(s):
1824961
PAR ID:
10288819
Author(s) / Creator(s):
;
Editor(s):
Althouse, Benjamin Muir
Date Published:
Journal Name:
PLOS Computational Biology
Volume:
17
Issue:
3
ISSN:
1553-7358
Page Range / eLocation ID:
e1008674
Format(s):
Medium: X
Sponsoring Org:
National Science Foundation
More Like this
  1. The spread of an infectious disease depends on intrinsic properties of the disease as well as the connectivity and actions of the population. This study investigates the dynamics of an SIR type model which accounts for human tendency to avoid infection while also maintaining preexisting, interpersonal relationships. Specifically, we use a network model in which individuals probabilistically deactivate connections to infected individuals and later reconnect to the same individuals upon recovery. To analyze this network model, a mean field approximation consisting of a system of fourteen ordinary differential equations for the number of nodes and edges is developed. This system of equations is closed using a moment closure approximation for the number of triple links. By analyzing the differential equations, it is shown that, in addition to force of infection and recovery rate, the probability of deactivating edges and the average node degree of the underlying network determine if an epidemic occurs. 
    more » « less
  2. In an epidemic network, lags due to travel time between populations, latent period, and recovery period can significantly change the epidemic behavior and result in successive echoing waves of the spread between various population clusters. Moreover, external shocks to a given population can propagate to other populations within the network, potentially snowballing into waves of resurgent epidemics. The main objective of this study is to investigate the effect of time delay and small shocks/uncertainties on the linear susceptible-infectious-susceptible (SIS) dynamics of epidemic networks. In this regard, the asymptotic stability of this class of networks is first studied, and then its performance loss due to small shocks/uncertainties is evaluated based on the notion of the norm. It is shown that network performance loss is correlated with the structure of the underlying graph, intrinsic time delays, epidemic characteristics, and external shocks. This performance measure is then used to develop an optimal traffic restriction algorithm for network performance enhancement, resulting in reduced infection in the metapopulation. A novel epidemic-based centrality index is also defined to evaluate the impact of every subpopulation on network performance, and its asymptotic behavior is investigated. It is shown that for specific choices of parameters, the output of the epidemic-based centrality index converges to the results obtained by local or eigenvector centralities. Moreover, given that epidemic-based centrality depends on the epidemic properties of the disease, it may yield distinct node rankings as the disease characteristics slowly change over time or as different types of infections spread. This node interlacing phenomenon is not observed in other centralities that rely solely on network structure. This unique characteristic of epidemic-based centrality enables it to adjust to various epidemic features. The derived centrality index is then adopted to improve the network robustness against external shocks on the epidemic network. The numerical results, along with the theoretical expectations, highlight the role of time delay as well as small shocks in investigating the most effective methods of epidemic containment. 
    more » « less
  3. We study the effect of population mobility on the transmission dynamics of infectious diseases by considering a susceptible-exposed-infectious-recovered (SEIR) epidemic model with graph Laplacian diffusion, that is, on a weighted network. First, we establish the existence and uniqueness of solutions to the SEIR model defined on a weighed graph. Then by constructing Liapunov functions, we show that the disease-free equilibrium is globally asymptotically stable if the basic reproduction number is less than unity and the endemic equilibrium is globally asymptotically stable if the basic reproduction number is greater than unity. Finally, we apply our generalized weighed graph to Watts–Strogatz network and carry out numerical simulations, which demonstrate that degrees of nodes determine peak numbers of the infectious population as well as the time to reach these peaks. It also indicates that the network has an impact on the transient dynamical behaviour of the epidemic transmission. 
    more » « less
  4. Abstract We define a bridge node to be a node whose neighbor nodes are sparsely connected to each other and are likely to be part of different components if the node is removed from the network. We propose a computationally light neighborhood-based bridge node centrality (NBNC) tuple that could be used to identify the bridge nodes of a network as well as rank the nodes in a network on the basis of their topological position to function as bridge nodes. The NBNC tuple for a node is asynchronously computed on the basis of the neighborhood graph of the node that comprises of the neighbors of the node as vertices and the links connecting the neighbors as edges. The NBNC tuple for a node has three entries: the number of components in the neighborhood graph of the node, the algebraic connectivity ratio of the neighborhood graph of the node and the number of neighbors of the node. We analyze a suite of 60 complex real-world networks and evaluate the computational lightness, effectiveness, efficiency/accuracy and uniqueness of the NBNC tuple vis-a-vis the existing bridgeness related centrality metrics and the Louvain community detection algorithm. 
    more » « less
  5. Abstract

    It is essential to study the robustness and centrality of interdependent networks for building reliable interdependent systems. Here, we consider a nonlinear load-capacity cascading failure model on interdependent networks, where the initial load distribution is not random, as usually assumed, but determined by the influence of each node in the interdependent network. The node influence is measured by an automated entropy-weighted multi-attribute algorithm that takes into account both different centrality measures of nodes and the interdependence of node pairs, then averaging for not only the node itself but also its nearest neighbors and next-nearest neighbors. The resilience of interdependent networks under such a more practical and accurate setting is thoroughly investigated for various network parameters, as well as how nodes from different layers are coupled and the corresponding coupling strength. The results thereby can help better monitoring interdependent systems.

     
    more » « less