We provide a systematic study of the problem of finding the source of a rumor in a network. We model rumor spreading in a network with a variant of the popular SIR model and then construct an estimator for the rumor source. This estimator is based upon a novel topological quantity which we term . We establish that this is an ML estimator for a class of graphs. We find the following surprising threshold phenomenon: on trees which grow faster than a line, the estimator always has non-trivial detection probability, whereas on trees that grow like a line, the detection probability will go to 0 as the network grows. Simulations performed on synthetic networks such as the popular small-world and scale-free networks, and on real networks such as an internet AS network and the U.S. electric power grid network, show that the estimator either finds the source exactly or within a few hops of the true source across different network topologies. We compare rumor centrality to another common network centrality notion known as distance centrality. We prove that on trees, the rumor center and distance center are equivalent, but on general networks, they may differ. Indeed, simulations show that rumor centrality outperforms distance centrality in finding rumor sources in networks which are not tree-like.
Prior work on rumor spreading has primarily focused on viral epidemics in populations. The natural (and somewhat standard) model for viral epidemics is known as the or SIR model @cite_13 . In this model, there are three types of nodes: (i) susceptible nodes, capable of being infected; (ii) infected nodes that can spread the virus further; and (iii) recovered nodes that are cured and can no longer become infected. Research in the SIR model has focused on understanding how the structure of the network and rates of infection cure lead to large epidemics @cite_0 , @cite_25 , @cite_26 , @cite_19 . This motivated various researchers to propose network inference techniques for learning the relevant network parameters @cite_16 , @cite_10 , @cite_4 , @cite_22 , @cite_5 . However, there has been little (or no) work done on inferring the source of an epidemic.
@cite_26 @cite_4 @cite_22 @cite_10 @cite_0 @cite_19 @cite_5 @cite_16 @cite_13 @cite_25
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Abstract A two-layer susceptible-infected-recovered unaware-aware (SIR-UA) epidemic model is presented to analyze the effect of different heterogeneous networks in a population. Random, scale-free, and small-world network topologies are tested to investigate the impact of awareness on the spread of epidemics in a two-layer network with diverse combinations of degree and structure. Susceptible and infected (both unaware and aware) individuals are associated with their neighboring nodes in a social network structure with various degree distributions. In the two-layer SIR-UA epidemic model, a virtual network represents the connections that spread information, while a physical network represents the physical social interactions that spread diseases. We test various combinations of network structures in virtual or physical networks, to understand the impact of information diffusion on the spread of epidemics in a heterogeneous network structure. Then, the effects of awareness on the spread of a disease are discussed. Finally, phase diagrams are illustrated to reveal the final regions covered by an epidemic with various network parameters. We find that a disease spreads less if the virtual social network is more connected than the network of physical connections. Besides the epidemic threshold, the recently proposed viral conductance @j by [11] may be regarded as an additional characterizer of the viral robustness of a network, that measures the overall ease in which viruses can spread in a particular network. Motivated to explain observed features of the viral conductance @j in simulations [29], we have analysed this metric in depth using the N-intertwined SIS epidemic model, that upper bounds the real infection probability in any network and, hence, provides safe-side bounds on which network protection can be based. Our study here derives a few exact results for @j, a number of different lower and upper bounds for @j with variable accuracy. We also extend the theory of the N-intertwined SIS epidemic model, by deducing formal series expansions of the steady-state fraction of infected nodes for any graph and any effective infection rate, that result in a series for the viral conductance @j. Though approximate, we illustrate here that the N-intertwined SIS epidemic model is so far the only SIS model on networks that is analytically tractable, and valuable to provide first order estimates of the epidemic impact in networks. Finally, inspired by the analogy between virus spread and synchronization of coupled oscillators in a network, we propose the synchronizability as the analogue of the viral conductance. Understanding the dynamics of computer virus (malware, worm) in cyberspace is an important problem that has attracted a fair amount of attention. Early investigations for this purpose adapted biological epidemic models, and thus inherited the so-called homogeneity assumption that each node is equally connected to others. Later studies relaxed this often unrealistic homogeneity assumption, but still focused on certain power-law networks. Recently, researchers investigated epidemic models in arbitrary networks (i.e., no restrictions on network topology). However, all these models only capture push-based infection, namely that an infectious node always actively attempts to infect its neighboring nodes. Very recently, the concept of pull-based infection was introduced but was not treated rigorously. Along this line of research, the present article investigates push- and pull-based epidemic spreading dynamics in arbitrary networks, using a nonlinear dynamical systems approach. The article advances the state-of-the-art as follows: (1) It presents a more general and powerful sufficient condition (also known as epidemic threshold in the literature) under which the spreading will become stable. (2) It gives both upper and lower bounds on the global mean infection rate, regardless of the stability of the spreading. (3) It offers insights into, among other things, the estimation of the global mean infection rate through localized monitoring of a small constant number of nodes, without knowing the values of the parameters. The effect of virus spreading in a telecommunication network, where a certain curing strategy is deployed, can be captured by epidemic models. In the N-intertwined model proposed and studied in [1], [2], the probability of each node to be infected depends on the curing and infection rate of its neighbors. In this paper, we consider the case where all infection rates are equal and different values of curing rates can be deployed within a given budget, in order to minimize the overall infection of the network. We investigate this difficult optimization together with a related problem where the curing budget must be minimized within a given level of network infection. Some properties of these problems are derived and several solution algorithms are proposed. These algorithms are compared on two real world network instances, while Erdos-Renyi graphs and some special graphs such as the cycle, the star, the wheel and the complete bipartite graph are also addressed. We study the problem of estimating the origin of an epidemic outbreak -- given a contact network and a snapshot of epidemic spread at a certain time, determine the infection source. Finding the source is important in different contexts of computer or social networks. We assume that the epidemic spread follows the most commonly used susceptible-infected-recovered model. We introduce an inference algorithm based on dynamic message-passing equations, and we show that it leads to significant improvement of performance compared to existing approaches. Importantly, this algorithm remains efficient in the case where one knows the state of only a fraction of nodes. How will a virus propagate in a real networkq How long does it take to disinfect a network given particular values of infection rate and virus death rateq What is the single best node to immunizeq Answering these questions is essential for devising network-wide strategies to counter viruses. In addition, viral propagation is very similar in principle to the spread of rumors, information, and “fads,” implying that the solutions for viral propagation would also offer insights into these other problem settings. We answer these questions by developing a nonlinear dynamical system (NLDS) that accurately models viral propagation in any arbitrary network, including real and synthesized network graphs. We propose a general epidemic threshold condition for the NLDS system: we prove that the epidemic threshold for a network is exactly the inverse of the largest eigenvalue of its adjacency matrix. Finally, we show that below the epidemic threshold, infections die out at an exponential rate. Our epidemic threshold model subsumes many known thresholds for special-case graphs (e.g., Erdos--Renyi, BA powerlaw, homogeneous). We demonstrate the predictive power of our model with extensive experiments on real and synthesized graphs, and show that our threshold condition holds for arbitrary graphs. Finally, we show how to utilize our threshold condition for practical uses: It can dictate which nodes to immunize; it can assess the effects of a throttling policy; it can help us design network topologies so that they are more resistant to viruses. Identifying influential nodes in complex networks has attracted much attention because of its great theoretical significance and wide application. Existing methods consider the edges equally when designing identifying methods for the unweighted networks. In this paper, we propose an edge weighting method based on adding the degree of its two end nodes and for the constructed weighted networks, we propose a weighted k-shell decomposition method (Wks). Further investigations on the epidemic spreading process of the Susceptible–Infected–Recovered (SIR) model and Susceptible–Infected (SI) model in real complex networks verify that our method is effective for detecting the node influence. The study of social networks, and in particular the spread of disease on networks, has attracted considerable recent attention in the physics community. In this paper, we show that a large class of standard epidemiological models, the so-called susceptible infective removed (SIR) models can be solved exactly on a wide variety of networks. In addition to the standard but unrealistic case of fixed infectiveness time and fixed and uncorrelated probability of transmission between all pairs of individuals, we solve cases in which times and probabilities are nonuniform and correlated. We also consider one simple case of an epidemic in a structured population, that of a sexually transmitted disease in a population divided into men and women. We confirm the correctness of our exact solutions with numerical simulations of SIR epidemics on networks. We investigate the effects of modular and temporal connectivity patterns on epidemic spreading. To this end, we introduce and analytically characterise a model of time-varying networks with tunable modularity. Within this framework, we study the epidemic size of Susceptible-Infected-Recovered, SIR, models and the epidemic threshold of Susceptible-Infected-Susceptible, SIS, models. Interestingly, we find that while the presence of tightly connected clusters inhibits SIR processes, it speeds up SIS phenomena. In this case, we observe that modular structures induce a reduction of the threshold with respect to time-varying networks without communities. We confirm the theoretical results by means of extensive numerical simulations both on synthetic graphs as well as on a real modular and temporal network. In a document network such as a citation network of scientific documents, web-logs, etc., the content produced by authors exhibits their interest in certain topics. In addition some authors influence other authors' interests. In this work, we propose to model the influence of cited authors along with the interests of citing authors. Moreover, we hypothesize that apart from the citations present in documents, the context surrounding the citation mention provides extra topical information about the cited authors. However, associating terms in the context to the cited authors remains an open problem. We propose novel document generation schemes that incorporate the context while simultaneously modeling the interests of citing authors and influence of the cited authors. Our experiments show significant improvements over baseline models for various evaluation criteria such as link prediction between document and cited author, and quantitatively explaining unseen text. To understand the current extent of the computer virus problem and predict its future course, the authors have conducted a statistical analysis of computer virus incidents in a large, stable sample population of PCs and developed new epidemiological models of computer virus spread. Only a small fraction of all known viruses have appeared in real incidents, partly because many viruses are below the theoretical epidemic threshold. The observed sub-exponential rate of viral spread can be explained by models of localized software exchange. A surprisingly small fraction of machines in well-protected business environments are infected. This may be explained by a model in which, once a machine is found to be infected, neighboring machines are checked for viruses. This kill signal idea could be implemented in networks to greatly reduce the threat of viral spread. A similar principle has been incorporated into a cost-effective anti-virus policy for organizations which works quite well in practice. > Scholars are increasingly citing electronic “web references” which are not preserved in libraries or full text archives. WebCite is a new standard for citing web references. To “webcite” a document involves archiving the cited Web page through www.webcitation.org and citing the WebCite permalink instead of (or in addition to) the unstable live Web page. This journal has amended its “instructions for authors” accordingly, asking authors to archive cited Web pages before submitting a manuscript. Almost 200 other journals are already using the system. We discuss the rationale for WebCite, its technology, and how scholars, editors, and publishers can benefit from the service. Citing scholars initiate an archiving process of all cited Web references, ideally before they submit a manuscript. Authors of online documents and websites which are expected to be cited by others can ensure that their work is permanently available by creating an archived copy using WebCite and providing the citation information including the WebCite link on their Web document(s). Editors should ask their authors to cache all cited Web addresses (Uniform Resource Locators, or URLs) “prospectively” before submitting their manuscripts to their journal. Editors and publishers should also instruct their copyeditors to cache cited Web material if the author has not done so already. Finally, WebCite can process publisher submitted “citing articles” (submitted for example as eXtensible Markup Language [XML] documents) to automatically archive all cited Web pages shortly before or on publication. Finally, WebCite can act as a focussed crawler, caching retrospectively references of already published articles. Copyright issues are addressed by honouring respective Internet standards (robot exclusion files, no-cache and no-archive tags). Long-term preservation is ensured by agreements with libraries and digital preservation organizations. The resulting WebCite Index may also have applications for research assessment exercises, being able to measure the impact of Web services and published Web documents through access and Web citation metrics. @PARASPLIT [J Med Internet Res 2005;7(5):e60] A citing sentence is one that appears in a scientific article and cites previous work. Citing sentences have been studied and used in many applications. For example, they have been used in scientific paper summarization, automatic survey generation, paraphrase identification, and citation function classification. Citing sentences that cite multiple papers are common in scientific writing. This observation should be taken into consideration when using citing sentences in applications. For instance, when a citing sentence is used in a summary of a scientific paper, only the fragments of the sentence that are relevant to the summarized paper should be included in the summary. In this paper, we present and compare three different approaches for identifying the fragments of a citing sentence that are related to a given target reference. Our methods are: word classification, sequence labeling, and segment classification. Our experiments show that segment classification achieves the best results. Epidemic outbreaks in human populations are facilitated by the underlying transportation network. We consider strategies for containing a viral spreading process by optimally allocating a limited budget to three types of protection resources: (i) Traffic control resources, (ii), preventative resources and (iii) corrective resources. Traffic control resources are employed to impose restrictions on the traffic flowing across directed edges in the transportation network. Preventative resources are allocated to nodes to reduce the probability of infection at that node (e.g. vaccines), and corrective resources are allocated to nodes to increase the recovery rate at that node (e.g. antidotes). We assume these resources have monetary costs associated with them, from which we formalize an optimal budget allocation problem which maximizes containment of the infection. We present a polynomial time solution to the optimal budget allocation problem using Geometric Programming (GP) for an arbitrary weighted and directed contact network and a large class of resource cost functions. We illustrate our approach by designing optimal traffic control strategies to contain an epidemic outbreak that propagates through a real-world air transportation network. We propose and solve exactly a model of a network that has both a tunable degree distribution and a tunable clustering coefficient. Among other things, our results indicate that increased clustering leads to a decrease in the size of the giant component of the network. We also study susceptible infective recovered type epidemic processes within the model and find that clustering decreases the size of epidemics, but also decreases the epidemic threshold, making it easier for diseases to spread. In addition, clustering causes epidemics to saturate sooner, meaning that they infect a near-maximal fraction of the network for quite low transmission rates. We consider the problem of reconstructing an epidemic over time, or, more general, reconstructing the propagation of an activity in a network. Our input consists of a temporal network, which contains information about when two nodes interacted, and a sample of nodes that have been reported as infected. The goal is to recover the flow of the spread, including discovering the starting nodes, and identifying other likely-infected nodes that are not reported. The problem we consider has multiple applications, from public health to social media and viral marketing purposes. Previous work explicitly factor-in many unrealistic assumptions: it is assumed that (a) the underlying network does not change;(b) we have access to perfect noise-free data; or (c) we know the exact propagation model. In contrast, we avoid these simplifications: we take into account the temporal network, we require only a small sample of reported infections, and we do not make any restrictive assumptions about the propagation model. We develop CulT, a scalable and effective algorithm to reconstruct epidemics that is also suited for online settings. CulT works by formulating the problem as that of a temporal Steiner-tree computation, for which we design a fast algorithm leveraging the specific problem structure. We demonstrate the efficacy of the proposed approach through extensive experiments on diverse datasets. Many network phenomena are well modeled as spreads of epidemics through a network. Prominent examples include the spread of worms and email viruses, and, more generally, faults. Many types of information dissemination can also be modeled as spreads of epidemics. In this paper we address the question of what makes an epidemic either weak or potent. More precisely, we identify topological properties of the graph that determine the persistence of epidemics. In particular, we show that if the ratio of cure to infection rates is larger than the spectral radius of the graph, then the mean epidemic lifetime is of order log n, where n is the number of nodes. Conversely, if this ratio is smaller than a generalization of the isoperimetric constant of the graph, then the mean epidemic lifetime is of order e sup na , for a positive constant a. We apply these results to several network topologies including the hypercube, which is a representative connectivity graph for a distributed hash table, the complete graph, which is an important connectivity graph for BGP, and the power law graph, of which the AS-level Internet graph is a prime example. We also study the star topology and the Erdos-Renyi graph as their epidemic spreading behaviors determine the spreading behavior of power law graphs. Identifying the most influential individuals spreading ideas, information, or infectious diseases is a topic receiving significant attention from network researchers, since such identification can assist or hinder information dissemination, product exposure, and contagious disease detection. Hub nodes, high betweenness nodes, high closeness nodes, and high k-shell nodes have been identified as good initial spreaders. However, few efforts have been made to use node diversity within network structures to measure spreading ability. The two-step framework described in this paper uses a robust and reliable measure that combines global diversity and local features to identify the most influential network nodes. Results from a series of Susceptible–Infected–Recovered (SIR) epidemic simulations indicate that our proposed method performs well and stably in single initial spreader scenarios associated with various complex network datasets. Purpose – The purpose of this paper is to suggest an alternative to the widely used Times Cited criterion for analysing citation networks. The approach involves taking account of the natures of the papers that cite a given paper, so as to differentiate between papers that attract the same number of citations.Design methodology approach – ArticleRank is an algorithm that has been derived from Google's PageRank algorithm to measure the influence of journal articles. ArticleRank is applied to two datasets – a citation network based on an early paper on webometrics, and a self‐citation network based on the 19 most cited papers in the Journal of Documentation – using citation data taken from the Web of Knowledge database.Findings – ArticleRank values provide a different ranking of a set of papers from that provided by the corresponding Times Cited values, and overcomes the inability of the latter to differentiate between papers with the same numbers of citations. The difference in rankings between Times Cited ... Finding the infection sources in a network when we only know the network topology and infected nodes, but not the rates of infection, is a challenging combinatorial problem, and it is even more difficult in practice where the underlying infection spreading model is usually unknown a priori . In this paper, we are interested in finding a source estimator that is applicable to various spreading models, including the susceptible–infected (SI), susceptible–infected–recovered (SIR), susceptible–infected–recovered–infected (SIRI), and susceptible–infected–susceptible (SIS) models. We show that under the SI, SIR, and SIRI spreading models and with mild technical assumptions, the Jordan center is the infection source associated with the most likely infection path in a tree network with a single infection source. This conclusion applies for a wide range of spreading parameters, while it holds for regular trees under the SIS model with homogeneous infection and recovery rates. Since the Jordan center does not depend on the infection, recovery, and reinfection rates, it can be regarded as a universal source estimator. We also consider the case where there are @math infection sources, generalize the Jordan center definition to a @math -Jordan center set, and show that this is an optimal infection source set estimator in a tree network for the SI model. Simulation results on various general synthetic networks and real-world networks suggest that Jordan center-based estimators consistently outperform the betweenness, closeness, distance, degree, eigenvector, and pagerank centrality-based heuristics, even if the network is not a tree.