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Journal ArticleDOI

Networks and epidemic models.

22 Sep 2005-Journal of the Royal Society Interface (The Royal Society)-Vol. 2, Iss: 4, pp 295-307
TL;DR: A variety of methods are described that allow the mixing network, or an approximation to the network, to be ascertained and how the two fields of network theory and epidemiological modelling can deliver an improved understanding of disease dynamics and better public health through effective disease control are suggested.
Abstract: Networks and the epidemiology of directly transmitted infectious diseases are fundamentally linked. The foundations of epidemiology and early epidemiological models were based on population wide random-mixing, but in practice each individual has a finite set of contacts to whom they can pass infection; the ensemble of all such contacts forms a ‘mixing network’. Knowledge of the structure of the network allows models to compute the epidemic dynamics at the population scale from the individual-level behaviour of infections. Therefore, characteristics of mixing networks—and how these deviate from the random-mixing norm—have become important applied concerns that may enhance the understanding and prediction of epidemic patterns and intervention measures. Here, we review the basis of epidemiological theory (based on random-mixing models) and network theory (based on work from the social sciences and graph theory). We then describe a variety of methods that allow the mixing network, or an approximation to the network, to be ascertained. It is often the case that time and resources limit our ability to accurately find all connections within a network, and hence a generic understanding of the relationship between network structure and disease dynamics is needed. Therefore, we review some of the variety of idealized network types and approximation techniques that have been utilized to elucidate this link. Finally, we look to the future to suggest how the two fields of network theory and epidemiological modelling can deliver an improved understanding of disease dynamics and better public health through effective disease control.

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Citations
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Proceedings ArticleDOI
22 Jan 2006
TL;DR: Some of the major results in random graphs and some of the more challenging open problems are reviewed, including those related to the WWW.
Abstract: We will review some of the major results in random graphs and some of the more challenging open problems. We will cover algorithmic and structural questions. We will touch on newer models, including those related to the WWW.

7,116 citations

Journal ArticleDOI
TL;DR: A coherent and comprehensive review of the vast research activity concerning epidemic processes is presented, detailing the successful theoretical approaches as well as making their limits and assumptions clear.
Abstract: Complex networks arise in a wide range of biological and sociotechnical systems. Epidemic spreading is central to our understanding of dynamical processes in complex networks, and is of interest to physicists, mathematicians, epidemiologists, and computer and social scientists. This review presents the main results and paradigmatic models in infectious disease modeling and generalized social contagion processes.

3,173 citations


Cites background from "Networks and epidemic models."

  • ...…different disciplines, and in the last ten years an impressive array of methods and approaches ranging from mean-field theories to rigorous results have provided new quantitative insights on the dynamics of contagion processes in complex networks (Danon et al., 2011; Keeling and Eames, 2005)....

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Journal ArticleDOI
TL;DR: In this article, the authors analyze data on the sexual behavior of a random sample of individuals, and find that the cumulative distributions of the number of sexual partners during the twelve months prior to the survey decays as a power law with similar exponents for females and males.
Abstract: Many ``real-world'' networks are clearly defined while most ``social'' networks are to some extent subjective. Indeed, the accuracy of empirically-determined social networks is a question of some concern because individuals may have distinct perceptions of what constitutes a social link. One unambiguous type of connection is sexual contact. Here we analyze data on the sexual behavior of a random sample of individuals, and find that the cumulative distributions of the number of sexual partners during the twelve months prior to the survey decays as a power law with similar exponents $\alpha \approx 2.4$ for females and males. The scale-free nature of the web of human sexual contacts suggests that strategic interventions aimed at preventing the spread of sexually-transmitted diseases may be the most efficient approach.

1,476 citations

Journal ArticleDOI
30 Apr 2008-PLOS ONE
TL;DR: A precise measure of ‘small-world-ness’ S is defined based on the trade off between high local clustering and short path length and several key properties of the metric are described and the use of WS canonical models is placed on a more secure footing.
Abstract: Background: Many technological, biological, social, and information networks fall into the broad class of 'small-world' networks: they have tightly interconnected clusters of nodes, and a shortest mean path length that is similar to a matched random graph (same number of nodes and edges). This semi-quantitative definition leads to a categorical distinction ('small/not-small') rather than a quantitative, continuous grading of networks, and can lead to uncertainty about a network's small-world status. Moreover, systems described by small-world networks are often studied using an equivalent canonical network model-the Watts-Strogatz (WS) model. However, the process of establishing an equivalent WS model is imprecise and there is a pressing need to discover ways in which this equivalence may be quantified. Methodology/Principal Findings: We defined a precise measure of 'small-world-ness' S based on the trade off between high local clustering and short path length. A network is now deemed a 'small-world' if S. 1-an assertion which may be tested statistically. We then examined the behavior of S on a large data-set of real-world systems. We found that all these systems were linked by a linear relationship between their S values and the network size n. Moreover, we show a method for assigning a unique Watts-Strogatz (WS) model to any real-world network, and show analytically that the WS models associated with our sample of networks also show linearity between S and n. Linearity between S and n is not, however, inevitable, and neither is S maximal for an arbitrary network of given size. Linearity may, however, be explained by a common limiting growth process. Conclusions/Significance: We have shown how the notion of a small-world network may be quantified. Several key properties of the metric are described and the use of WS canonical models is placed on a more secure footing.

1,211 citations


Cites methods from "Networks and epidemic models."

  • ...One canonical model used as a candidate for network equivalence is the original Watts-Strogatz (WS) model, which has been used as a substrate for studying dynamics in the diverse fields of ecology [8], economics [9,10], epidemiology [11,12], and neuroscience [13]....

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Journal ArticleDOI
TL;DR: Historical, epidemiologic, theoretical, and pragmatic public health perspectives on the concept of herd immunity are provided.
Abstract: The term "herd immunity" is widely used but carries a variety of meanings. Some authors use it to describe the proportion immune among individuals in a population. Others use it with reference to a particular threshold proportion of immune individuals that should lead to a decline in incidence of infection. Still others use it to refer to a pattern of immunity that should protect a population from invasion of a new infection. A common implication of the term is that the risk of infection among susceptible individuals in a population is reduced by the presence and proximity of immune individuals (this is sometimes referred to as "indirect protection" or a "herd effect"). We provide brief historical, epidemiologic, theoretical, and pragmatic public health perspectives on this concept.

973 citations


Cites background from "Networks and epidemic models."

  • ...This nonrandom mixing can in theory be described through the use of network models that include more detail information about who mixes with whom [26]....

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References
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Journal ArticleDOI
04 Jun 1998-Nature
TL;DR: Simple models of networks that can be tuned through this middle ground: regular networks ‘rewired’ to introduce increasing amounts of disorder are explored, finding that these systems can be highly clustered, like regular lattices, yet have small characteristic path lengths, like random graphs.
Abstract: Networks of coupled dynamical systems have been used to model biological oscillators, Josephson junction arrays, excitable media, neural networks, spatial games, genetic control networks and many other self-organizing systems. Ordinarily, the connection topology is assumed to be either completely regular or completely random. But many biological, technological and social networks lie somewhere between these two extremes. Here we explore simple models of networks that can be tuned through this middle ground: regular networks 'rewired' to introduce increasing amounts of disorder. We find that these systems can be highly clustered, like regular lattices, yet have small characteristic path lengths, like random graphs. We call them 'small-world' networks, by analogy with the small-world phenomenon (popularly known as six degrees of separation. The neural network of the worm Caenorhabditis elegans, the power grid of the western United States, and the collaboration graph of film actors are shown to be small-world networks. Models of dynamical systems with small-world coupling display enhanced signal-propagation speed, computational power, and synchronizability. In particular, infectious diseases spread more easily in small-world networks than in regular lattices.

39,297 citations


"Networks and epidemic models." refers background in this paper

  • ...The high level of clustering means that most infection occurs locally, but short path lengths mean that epidemic spread through the network is rapid and disease is unlikely to be contained within small regions of the population ( Watts & Strogatz 1998 )....

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  • ...Small-world networks, described in the work of Watts & Strogatz (1998; see also Watts 1999), offer a means of moving between the rigid arrangement of lattices and the unstructured connections of random networks....

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  • ...While collecting network data is beset with difficulties, the simulation of disease transmission on networks is relatively straightforward (Eames & Keeling 2002; Eubank et al. 2004; Meyers et al. 2005; Read & Keeling 2003; Wallinga et al. 1999; Watts & Strogatz 1998 ), relying on the observation that...

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  • ...…mixing networks, the concepts underlying percolation theory are immediately relevant to epidemiology, and many of these ideas and the tools for understanding them have been applied in epidemiological settings (Mollison 1977; Grassberger 1983; Newman & Watts 1999; Newman 2002; Warren et al. 2002)....

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  • ...On a much smaller scale are gene and neural networks, which display the high clustering and low path lengths associated with the small-world model ( Watts & Strogatz 1998 )....

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Journal ArticleDOI
15 Oct 1999-Science
TL;DR: A model based on these two ingredients reproduces the observed stationary scale-free distributions, which indicates that the development of large networks is governed by robust self-organizing phenomena that go beyond the particulars of the individual systems.
Abstract: Systems as diverse as genetic networks or the World Wide Web are best described as networks with complex topology. A common property of many large networks is that the vertex connectivities follow a scale-free power-law distribution. This feature was found to be a consequence of two generic mechanisms: (i) networks expand continuously by the addition of new vertices, and (ii) new vertices attach preferentially to sites that are already well connected. A model based on these two ingredients reproduces the observed stationary scale-free distributions, which indicates that the development of large networks is governed by robust self-organizing phenomena that go beyond the particulars of the individual systems.

33,771 citations


"Networks and epidemic models." refers background in this paper

  • ...In many observed networks, this is far from homogeneous; it is often the case that many individuals have a small number of neighbours, while a few have significantly more connections (Albert et al. 1999; Barabási & Albert 1999; Jeong et al. 2000; Liljeros et al. 2001)....

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  • ...Scale-free networks can be constructed dynamically by adding new individuals to a network one by one with a connection mechanism that mimics the natural formation of social contacts (Barabási & Albert 1999;Albert et al. 2000; Pastor-Satorras & Vespignani 2001)....

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  • ...This property was initially observed for worldwide Web connections (Albert et al. 1999), but has also been reported in power grid networks, graphs of actor collaborations (Barabási & Albert 1999) and networks of human sexual contacts (Liljeros et al. 2001)....

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  • ...In the preferential attachment model of Barabási & Albert (1999), the existence of individuals of arbitrarily large degree means that there is no level of random vaccination that is sufficient to prevent an epidemic (Albert et al. 2000; Lloyd&May 2001; Pastor-Satorras& Vespignani 2001)....

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Book
25 Nov 1994
TL;DR: This paper presents mathematical representation of social networks in the social and behavioral sciences through the lens of Dyadic and Triadic Interaction Models, which describes the relationships between actor and group measures and the structure of networks.
Abstract: Part I. Introduction: Networks, Relations, and Structure: 1. Relations and networks in the social and behavioral sciences 2. Social network data: collection and application Part II. Mathematical Representations of Social Networks: 3. Notation 4. Graphs and matrixes Part III. Structural and Locational Properties: 5. Centrality, prestige, and related actor and group measures 6. Structural balance, clusterability, and transitivity 7. Cohesive subgroups 8. Affiliations, co-memberships, and overlapping subgroups Part IV. Roles and Positions: 9. Structural equivalence 10. Blockmodels 11. Relational algebras 12. Network positions and roles Part V. Dyadic and Triadic Methods: 13. Dyads 14. Triads Part VI. Statistical Dyadic Interaction Models: 15. Statistical analysis of single relational networks 16. Stochastic blockmodels and goodness-of-fit indices Part VII. Epilogue: 17. Future directions.

17,104 citations

Book
01 Jan 1969

16,023 citations


"Networks and epidemic models." refers background or methods in this paper

  • ...In this case, the network of relevant interactions would be a directed graph (Harary 1969; Bollobás 1979)....

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  • ...I N Z b I N : ð1:3Þ This leads to a nonlinear term (bSI/N ) representing the transmission of infection, generating a variety of rich dynamical behaviours (Schwartz 1985; Olsen et al. 1986; Rand & Wilson 1991; Anderson & May 1992; Earn et al. 2000; Keeling et al. 2001)....

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  • ...We can use an ‘adjacency matrix’ or ‘sociomatrix’, A, to describe the connections within a population (Harary 1969; Bollobás 1979; Wasserman & Faust 1994; West 1996); AijZ1 if there is a connection such that infection could pass from individual i to individual j ; otherwise, AijZ0....

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Journal ArticleDOI
TL;DR: In this article, the authors considered the problem of finding a causal factor which appears to be adequate to account for the magnitude of the frequent epidemics of disease which visit almost every population.
Abstract: (1) One of the most striking features in the study of epidemics is the difficulty of finding a causal factor which appears to be adequate to account for the magnitude of the frequent epidemics of disease which visit almost every population. It was with a view to obtaining more insight regarding the effects of the various factors which govern the spread of contagious epidemics that the present investigation was undertaken. Reference may here be made to the work of Ross and Hudson (1915-17) in which the same problem is attacked. The problem is here carried to a further stage, and it is considered from a point of view which is in one sense more general. The problem may be summarised as follows: One (or more) infected person is introduced into a community of individuals, more or less susceptible to the disease in question. The disease spreads from the affected to the unaffected by contact infection. Each infected person runs through the course of his sickness, and finally is removed from the number of those who are sick, by recovery or by death. The chances of recovery or death vary from day to day during the course of his illness. The chances that the affected may convey infection to the unaffected are likewise dependent upon the stage of the sickness. As the epidemic spreads, the number of unaffected members of the community becomes reduced. Since the course of an epidemic is short compared with the life of an individual, the population may be considered as remaining constant, except in as far as it is modified by deaths due to the epidemic disease itself. In the course of time the epidemic may come to an end. One of the most important probems in epidemiology is to ascertain whether this termination occurs only when no susceptible individuals are left, or whether the interplay of the various factors of infectivity, recovery and mortality, may result in termination, whilst many susceptible individuals are still present in the unaffected population. It is difficult to treat this problem in its most general aspect. In the present communication discussion will be limited to the case in which all members of the community are initially equally susceptible to the disease, and it will be further assumed that complete immunity is conferred by a single infection.

8,238 citations