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Register a new userRevealing latent factors of temporal networks for mesoscale intervention in epidemic spread
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The customary perspective to reason about epidemic mitigation in temporal networks hinges on the identification of nodes with specific features or network roles. The ensuing individual-based control strategies, however, are difficult to carry out in practice and ignore important correlations between topological and temporal patterns. Here we adopt a mesoscopic perspective and present a principled framework to identify collective features at multiple scales and rank their importance for epidemic spread. We use tensor decomposition techniques to build an additive representation of a temporal network in terms of mesostructures, such as cohesive clusters and temporally-localized mixing patterns. This representation allows to determine the impact of individual mesostructures on epidemic spread and to assess the effect of targeted interventions that remove chosen structures. We illustrate this approach using high-resolution social network data on face-to-face interactions in a school and show that our method affords the design of effective mesoscale interventions.
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Temporal networks are widely used to represent a vast diversity of systems, including in particular social interactions, and the spreading processes unfolding on top of them. The identification of structures playing important roles in such processes remains largely an open question, despite recent progresses in the case of static networks. Here, we consider as candidate structures the recently introduced concept of span-cores: the span-cores decompose a temporal network into subgraphs of controlled duration and increasing connectivity, generalizing the core-decomposition of static graphs. To assess the relevance of such structures, we explore the effectiveness of strategies aimed either at containing or maximizing the impact of a spread, based respectively on removing span-cores of high cohesiveness or duration to decrease the epidemic risk, or on seeding the process from such structures. The effectiveness of such strategies is assessed in a variety of empirical data sets and compared to baselines that use only static information on the centrality of nodes and static concepts of coreness, as well as to a baseline based on a temporal centrality measure. Our results show that the most stable and cohesive temporal cores play indeed an important role in epidemic processes on temporal networks, and that their nodes are likely to represent influential spreaders.
Time-varying network topologies can deeply influence dynamical processes mediated by them. Memory effects in the pattern of interactions among individuals are also known to affect how diffusive and spreading phenomena take place. In this paper we analyze the combined effect of these two ingredients on epidemic dynamics on networks. We study the susceptible-infected-susceptible (SIS) and the susceptible-infected-removed (SIR) models on the recently introduced activity-driven networks with memory. By means of an activity-based mean-field approach we derive, in the long time limit, analytical predictions for the epidemic threshold as a function of the parameters describing the distribution of activities and the strength of the memory effects. Our results show that memory reduces the threshold, which is the same for SIS and SIR dynamics, therefore favouring epidemic spreading. The theoretical approach perfectly agrees with numerical simulations in the long time asymptotic regime. Strong aging effects are present in the preasymptotic regime and the epidemic threshold is deeply affected by the starting time of the epidemics. We discuss in detail the origin of the model-dependent preasymptotic corrections, whose understanding could potentially allow for epidemic control on correlated temporal networks.
Dynamic networks exhibit temporal patterns that vary across different time scales, all of which can potentially affect processes that take place on the network. However, most data-driven approaches used to model time-varying networks attempt to capture only a single characteristic time scale in isolation --- typically associated with the short-time memory of a Markov chain or with long-time abrupt changes caused by external or systemic events. Here we propose a unified approach to model both aspects simultaneously, detecting short and long-time behaviors of temporal networks. We do so by developing an arbitrary-order mixed Markov model with change points, and using a nonparametric Bayesian formulation that allows the Markov order and the position of change points to be determined from data without overfitting. In addition, we evaluate the quality of the multiscale model in its capacity to reproduce the spreading of epidemics on the temporal network, and we show that describing multiple time scales simultaneously has a synergistic effect, where statistically significant features are uncovered that otherwise would remain hidden by treating each time scale independently.
One of the popular dynamics on complex networks is the epidemic spreading. An epidemic model describes how infections spread throughout a network. Among the compartmental models used to describe epidemics, the Susceptible-Infected-Susceptible (SIS) model has been widely used. In the SIS model, each node can be susceptible, become infected with a given infection rate, and become again susceptible with a given curing rate. In this paper, we add a new compartment to the classic SIS model to account for human response to epidemic spread. Each individual can be infected, susceptible, or alert. Susceptible individuals can become alert with an alerting rate if infected individuals exist in their neighborhood. An individual in the alert state is less probable to become infected than an individual in the susceptible state; due to a newly adopted cautious behavior. The problem is formulated as a continuous-time Markov process on a general static graph and then modeled into a set of ordinary differential equations using mean field approximation method and the corresponding Kolmogorov forward equations. The model is then studied using results from algebraic graph theory and center manifold theorem. We analytically show that our model exhibits two distinct thresholds in the dynamics of epidemic spread. Below the first threshold, infection dies out exponentially. Beyond the second threshold, infection persists in the steady state. Between the two thresholds, the infection spreads at the first stage but then dies out asymptotically as the result of increased alertness in the network. Finally, simulations are provided to support our findings. Our results suggest that alertness can be considered as a strategy of controlling the epidemics which propose multiple potential areas of applications, from infectious diseases mitigations to malware impact reduction.
Vaccination is an important measure available for preventing or reducing the spread of infectious diseases. In this paper, an epidemic model including susceptible, infected, and imperfectly vaccinated compartments is studied on Watts-Strogatz small-world, Barabasi-Albert scale-free, and random scale-free networks. The epidemic threshold and prevalence are analyzed. For small-world networks, the effective vaccination intervention is suggested and its influence on the threshold and prevalence is analyzed. For scale-free networks, the threshold is found to be strongly dependent both on the effective vaccination rate and on the connectivity distribution. Moreover, so long as vaccination is effective, it can linearly decrease the epidemic prevalence in small-world networks, whereas for scale-free networks it acts exponentially. These results can help in adopting pragmatic treatment upon diseases in structured populations.
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