A systematic framework of modelling epidemics on temporal networks

Most real networks are characterized by connectivity patterns that evolve in time following complex, non-Markovian, dynamics. Here we investigate the impact of this ubiquitous feature by studying the Susceptible-Infected-Recovered (SIR) and Susceptible-Infected-Susceptible (SIS) epidemic models on activity driven networks with and without memory (i.e., Markovian and non-Markovian). We show that while memory inhibits the spreading process in SIR models, where the epidemic threshold is moved to larger values, it plays the opposite effect in the case of the SIS, where the threshold is lowered. The heterogeneity in tie strengths, and the frequent repetition of connections that it entails, allows in fact less virulent SIS-like diseases to survive in tightly connected local clusters that serve as reservoir for the virus. We validate this picture by evaluating the threshold of both processes in a real temporal network. Our findings confirm the important role played by non-Markovian network dynamics on dynamical processes

A Susceptible Infective Recovered (SIR) model is usually unable to mimic the actual epidemiological system exactly. The reasons for this inaccuracy include observation errors and model discrepancies due to assumptions and simplifications made by the SIR model. Hence, this work proposes calibration and prediction methods for the SIR model with a one-time reported number of infected cases. Given that the observation errors of the reported data are assumed to be heteroscedastic, we propose two predictors to predict the actual epidemiological system by modeling the model discrepancy through a Gaussian Process model. One is the calibrated SIR model, and the other one is the discrepancy-corrected predictor, which integrates the calibrated SIR model with the Gaussian Process predictor to solve the model discrepancy. A wild bootstrap method quantifies the two predictors' uncertainty, while two numerical studies assess the performance of the proposed method. The numerical results show that, the proposed predictors outperform the existing ones and the prediction accuracy of the discrepancy-corrected predictor is improved by at least 49.95%.

Susceptible-infectious-recovered models revisited: From the individual level to the population level

We present a contact-based model to study the spreading of epidemics by means of extending the dynamic message-passing approach to temporal networks. The shift in perspective from node- to edge-centric quantities enables accurate modeling of Markovian susceptible-infected-recovered outbreaks on time-varying trees, i.e., temporal networks with a loop-free underlying topology. On arbitrary graphs, the proposed contact-based model incorporates potential structural and temporal heterogeneities of the contact network and improves analytic estimations with respect to the individual-based (node-centric) approach at a low computational and conceptual cost. Within this new framework, we derive an analytical expression for the epidemic threshold on temporal networks and demonstrate the feasibility of this method on empirical data.

The classic susceptible-infectious-recovered (SIR) model, has been used extensively to study the dynamical evolution of an infectious disease in a large population. The SIR-susceptible (SIRS) model is an extension of the SIR model to allow modeling imperfect immunity (those who have recovered might become susceptible again). SIR(S) models assume observed counts are “mass balanced.” Here, mass balance means that total count equals the sum of counts of the individual components of the model. However, since the observed counts have errors, we propose a model that assigns the mass balance to the hidden process of a (Bayesian) hierarchical SIRS (HSIRS) model. Another challenge is to capture the stochastic or random nature of an epidemic process in a SIRS. The HSIRS model accomplishes this through modeling the dynamical evolution on a transformed scale. Through simulation, we compare the HSIRS model to the classic SIRS model, a model where it is assumed that the observed counts are mass balanced and the dynamical evolution is deterministic.

In order to meet passengers’ demands for increasing travel efficiency, the structure of China’s airport network will become more and more complex, and its operating environment has become more complex, so, it is important to measure the robustness of China’s airport network under the influence of complex disturbance factors. This paper proposes an airport network robustness analysis method based on the multi-layer temporal complex network model (MTNM) by introducing the time attribute. Firstly, we establish the network structure characteristics such as temporal degree, temporal closeness centrality (TC), and temporal betweenness centrality (TB) of airport network nodes, and take temporal network efficiency and temporal maximum connected subgraph as indicators; then inflection points of loss fitting curves for temporal network characteristics metrics under random attacks and deliberate attacks can be identified to evaluate network robustness. The results show that compared with static network, using multi-layer temporal network model can describe the performance characteristics of the network more accurately.

In the study of infectious diseases on networks, researchers calculate epidemic thresholds to help forecast whether or not a disease will eventually infect a large fraction of a population. Because network structure typically changes with time, which fundamentally influences the dynamics of spreading processes and in turn affects epidemic thresholds for disease propagation, it is important to examine epidemic thresholds in models of disease spread on temporal networks. Most existing studies of epidemic thresholds in temporal networks have focused on models in discrete time, but most real-world networked systems evolve continuously with time. In our work, we encode the continuous time-dependence of networks in the evaluation of the epidemic threshold of a susceptible–infected–susceptible (SIS) process by studying an SIS model on tie-decay networks. We derive the epidemic-threshold condition of this model, and we perform numerical experiments to verify it. We also examine how different factors—the decay coefficients of the tie strengths in a network, the frequency of the interactions between the nodes in the network, and the sparsity of the underlying social network on which interactions occur—lead to decreases or increases of the critical values of the threshold and hence contribute to facilitating or impeding the spread of a disease. We thereby demonstrate how the features of tie-decay networks alter the outcome of disease spread.

The Susceptible-Infectious-Recovered (SIR) model is the canonical model of epidemics of infections that make people immune upon recovery. Many of the open questions in computational epidemiology concern the underlying contact structure's impact on models like the SIR model. Temporal networks constitute a theoretical framework capable of encoding structures both in the networks of who could infect whom and when these contacts happen. In this article, we discuss the detailed assumptions behind such simulations-how to make them comparable with analytically tractable formulations of the SIR model, and at the same time, as realistic as possible. We also present a highly optimized, open-source code for this purpose and discuss all steps needed to make the program as fast as possible.

Identifying influential spreaders is an important issue for capturing the dynamics of information diffusion in temporal networks. Most of the identification of influential spreaders in previous researches were focused on analysing static networks, rarely highlighted on dynamics. However, those measures which are proposed for static topologies only, unable to faithfully capture the effect of temporal variations on the importance of nodes. In this paper, a shortest temporal path algorithm is proposed for calculating the minimum time that information interaction between nodes. This algorithm can effectively find out the shortest temporal path when considering the network integrity. On the basis of this, the temporal efficiency centrality (TEC) algorithm in temporal networks is proposed, which identify influential nodes by removing each node and taking the variation of the whole network into consideration at the same time. To evaluate the effectiveness of this algorithm, we conduct the experiment on four real-world temporal networks for Susceptible-Infected-Recovered (SIR) model. By employing the imprecision and the Kendall’s au coefficient, The results show that this algorithm can effectively evaluate the importance of nodes in temporal networks.

Predicting the diffusion of real-world contagion processes requires a simplified description of human-to-human interactions. Temporal networks offer a powerful means to develop such a mathematically-transparent description. Through temporal networks, one may analytically study the co-evolution of the contagion process and the network topology, as well as incorporate realistic feedback-loop mechanisms related to individual behavioral changes to the contagion. Despite considerable progress, the state-of-the-art does not allow for studying general time-varying networks, where links between individuals dynamically switch to reflect the complexity of social behavior. Here, we tackle this problem by considering a temporal network, in which reducible, associated with node-specific properties, and irreducible links, describing dyadic social ties, simultaneously vary over time. We develop a general mean field theory for the Susceptible-Infected-Susceptible model and conduct an extensive numerical campaign to elucidate the role of network parameters on the average degree of the temporal network and the epidemic threshold. Specifically, we describe how the interplay between reducible and irreducible links influences the disease dynamics, offering insights towards the analysis of complex dynamical networks across science and engineering.

In this work we consider temporal networks, i.e. networks defined by a labelinglambda assigning to each edge of an underlying graphG a set of discrete time-labels. The labels of an edge, which are natural numbers, indicate the discrete time moments at which the edge is available. We focus on path problems of temporal networks. In particular, we consider time-respecting paths, i.e. paths whose edges are assigned by lambda a strictly increasing sequence of labels. We begin by giving two efficient algorithms for computing shortest time-respecting paths on a temporal network. We then prove that there is a natural analogue of Menger’s theorem holding for arbitrary temporal networks. Finally, we propose two cost minimization parameters for temporal network design. One is the temporality of G, in which the goal is to minimize the maximum number of labels of an edge, and the other is the temporal cost of G, in which the goal is to minimize the total number of labels used. Optimization of these parameters is performed subject to some connectivity constraint. We prove several lower and upper bounds for the temporality and the temporal cost of some very basic graph families such as rings, directed acyclic graphs, and trees.

Temporal networks come with a wide variety of heterogeneities, from burstiness of event sequences to correlations between timings of node and link activations. In this paper, we set to explore the latter by using greedy walks as probes of temporal network structure. Given a temporal network (a sequence of contacts), greedy walks proceed from node to node by always following the first available contact. Because of this, their structure is particularly sensitive to temporal-topological patterns involving repeated contacts between sets of nodes. This becomes evident in their small coverage per step as compared to a temporal reference model -- in empirical temporal networks, greedy walks often get stuck within small sets of nodes because of correlated contact patterns. While this may also happen in static networks that have pronounced community structure, the use of the temporal reference model takes the underlying static network structure out of the equation and indicates that there is a purely temporal reason for the observations. Further analysis of the structure of greedy walks indicates that burst trains, sequences of repeated contacts between node pairs, are the dominant factor. However, there are larger patterns too, as shown with non-backtracking greedy walks. We proceed further to study the entropy rates of greedy walks, and show that the sequences of visited nodes are more structured and predictable in original data as compared to temporally uncorrelated references. Taken together, these results indicate a richness of correlated temporal-topological patterns in temporal networks.

Studies on how to model the interplay between diseases and behavioral responses (so-called coupled disease-behavior interaction) have attracted increasing attention. Owing to the lack of obvious clinical evidence of diseases, or the incomplete information related to the disease, the risks of infection cannot be perceived and may lead to inappropriate behavioral responses. Therefore, how to quantitatively analyze the impacts of asymptomatic infection on the interplay between diseases and behavioral responses is of particular importance. In this letter, under the complex network framework, we study the coupled disease-behavior interaction model by dividing infectious individuals into two states: U-state (without evident clinical symptoms, labelled as U) and I-state (with evident clinical symptoms, labelled as I). A susceptible individual can be infected by U- or I-nodes, however, since the U-nodes cannot be easily observed, susceptible individuals take behavioral responses only when they contact I-nodes. The mechanism is considered in the improved Susceptible-Infected-Susceptible (SIS) model and the improved Susceptible-Infected-Recovered (SIR) model, respectively. Then, one of the most concerned problems in spreading dynamics: the epidemic thresholds for the two models are given by two methods. The analytic results quantitatively describe the influence of different factors, such as asymptomatic infection, the awareness rate, the network structure, and so forth, on the epidemic thresholds. Moreover, because of the irreversible process of the SIR model, the suppression effect of the improved SIR model is weaker than the improved SIS model.

We study cascades in social networks with the independent cascade (IC) model and the Susceptible-Infected-recovered (SIR) model. The well-studied IC model fails to capture the feature of node recovery, and the SIR model is a variant of the IC model with the node recovery feature. In the SIR model, by computing the probability that a node successfully infects another before its recovery and viewing this probability as the corresponding IC parameter, an equivalence between the two models is established, except that the events of the infections along different out-going edges of a node become dependent in the SIR model, whereas these events are independent in the IC model. In this paper, we thoroughly compare the two models and examine the effect of this extra dependency in the SIR model. By a carefully designed coupling argument, we show that the seeds in the IC model have a stronger influence spread than their counterparts in the SIR model, and sometimes it can be significantly stronger. Specifically, we prove that, given the same network, the same seed sets, and the parameters of the two models being set based on the above-mentioned equivalence, the expected number of infected nodes at the end of the cascade for the IC model is weakly larger than that for the SIR model, and there are instances where this dominance is significant. We also study the influence maximization problem (the optimization problem of selecting a set of nodes as initial seeds in a social network to maximize their influence) with the SIR model. We show that the above-mentioned difference in the two models yields different seed-selection strategies, which motivates the design of influence maximization algorithms specifically for the SIR model. We design efficient approximation algorithms with theoretical guarantees by adapting the reverse-reachable-set-based algorithms, commonly used for the IC model, to the SIR model.

The validity of the continuous susceptible-infected-recovered (SIR) is questioned. It is pointed out that the basic assumption used in the model equations is wrong. The classic SIR and susceptible-infected-recovered-susceptible (SIRS) models have the form of the state ordinary differential equation (ODE). These equations do not reflect the spatial distribution of individuals. Moreover, what is more important, the SIR model equations do not reflect the huge collective memory of the modeled system. Such issues as the probability distribution of the immunity period and other time intervals are not taken into account in the ODE SIR model. It is pointed out that the model results depend strongly on these distributions. A comparison to the agent-based model (ABM) and corresponding computer simulations is done. In the paper, the validity of SIR epidemics model is questioned, the deficiency and the basic assumptions of the SIR model are pointed out. This makes the existence of the corresponding differential equations doubtful.