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Register a new userSimplicial contagion in temporal higher-order networks
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Complex networks represent the natural backbone to study epidemic processes in populations of interacting individuals. Such a modeling framework, however, is naturally limited to pairwise interactions, making it less suitable to properly describe social contagion, where individuals acquire new norms or ideas after simultaneous exposure to multiple sources of infections. Simplicial contagion has been proposed as an alternative framework where simplices are used to encode group interactions of any order. The presence of higher-order interactions leads to explosive epidemic transitions and bistability which cannot be obtained when only dyadic ties are considered. In particular, critical mass effects can emerge even for infectivity values below the standard pairwise epidemic threshold, where the size of the initial seed of infectious nodes determines whether the system would eventually fall in the endemic or the healthy state. Here we extend simplicial contagion to time-varying networks, where pairwise and higher-order simplices can be created or destroyed over time. By following a microscopic Markov chain approach, we find that the same seed of infectious nodes might or might not lead to an endemic stationary state, depending on the temporal properties of the underlying network structure, and show that persistent temporal interactions anticipate the onset of the endemic state in finite-size systems. We characterize this behavior on higher-order networks with a prescribed temporal correlation between consecutive interactions and on heterogeneous simplicial complexes, showing that temporality again limits the effect of higher-order spreading, but in a less pronounced way than for homogeneous structures. Our work suggests the importance of incorporating temporality, a realistic feature of many real-world systems, into the investigation of dynamical processes beyond pairwise interactions.
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In this Chapter, we discuss the effects of higher-order structures on SIS-like processes of social contagion. After a brief motivational introduction where we illustrate the standard SIS process on networks and the difference between simple and complex contagions, we introduce spreading processes on higher-order structures starting from the most general formulation on hypergraphs and then moving to several mean-field and heterogeneous mean-field approaches. The results highlight the rich phenomenology brought by taking into account higher-order contagion effects: both continuous and discontinuous transitions are observed, and critical mass effects emerge. We conclude with a short discussion on the theoretical results regarding the nature of the epidemic transition and the general need for data to validate these models.
The propagation of information in social, biological and technological systems represents a crucial component in their dynamic behavior. When limited to pairwise interactions, a rather firm grip is available on the relevant parameters and critical transitions of these spreading processes, most notably the pandemic transition, which indicates the conditions for the spread to cover a large fraction of the network. The challenge is that, in many relevant applications, the spread is driven by higher order relationships, in which several components undergo a group interaction. To address this, we analyze the spreading dynamics in a simplicial complex environment, designed to capture the coexistence of interactions of different orders. We find that, while pairwise interactions play a key role in the initial stages of the spread, once it gains coverage, higher order simplices take over and drive the contagion dynamics. The result is a distinctive spreading phase diagram, exhibiting a discontinuous pandemic transition, and hence offering a qualitative departure from the traditional network spreading dynamics.
The metapopulation framework is adopted in a wide array of disciplines to describe systems of well separated yet connected subpopulations. The subgroups or patches are often represented as nodes in a network whose links represent the migration routes among them. The connections have been so far mostly considered as static, but in general evolve in time. Here we address this case by investigating simple contagion processes on time-varying metapopulation networks. We focus on the SIR process and determine analytically the mobility threshold for the onset of an epidemic spreading in the framework of activity-driven network models. We find profound differences from the case of static networks. The threshold is entirely described by the dynamical parameters defining the average number of instantaneously migrating individuals and does not depend on the properties of the static network representation. Remarkably, the diffusion and contagion processes are slower in time-varying graphs than in their aggregated static counterparts, the mobility threshold being even two orders of magnitude larger in the first case. The presented results confirm the importance of considering the time-varying nature of complex networks.
The vast majority of strategies aimed at controlling contagion processes on networks considers the connectivity pattern of the system as either quenched or annealed. However, in the real world many networks are highly dynamical and evolve in time concurrently to the contagion process. Here, we derive an analytical framework for the study of control strategies specifically devised for time-varying networks. We consider the removal/immunization of individual nodes according the their activity in the network and develop a block variable mean-field approach that allows the derivation of the equations describing the evolution of the contagion process concurrently to the network dynamic. We derive the critical immunization threshold and assess the effectiveness of the control strategies. Finally, we validate the theoretical picture by simulating numerically the information spreading process and control strategies in both synthetic networks and a large-scale, real-world mobile telephone call dataset
Simple models of infectious diseases tend to assume random mixing of individuals, but real interactions are not random pairwise encounters: they occur within various types of gatherings such as workplaces, households, schools, and concerts, best described by a higher-order network structure. We model contagions on higher-order networks using group-based approximate master equations, in which we track all states and interactions within a group of nodes and assume a mean-field coupling between them. Using the Susceptible-Infected-Susceptible dynamics, our approach reveals the existence of a mesoscopic localization regime, where a disease can concentrate and self-sustain only around large groups in the network overall organization. In this regime, the phase transition is smeared, characterized by an inhomogeneous activation of the groups. At the mesoscopic level, we observe that the distribution of infected nodes within groups of a same size can be very dispersed, even bimodal. When considering heterogeneous networks, both at the level of nodes and groups, we characterize analytically the region associated with mesoscopic localization in the structural parameter space. We put in perspective this phenomenon with eigenvector localization and discuss how a focus on higher-order structures is needed to discern the more subtle localization at the mesoscopic level. Finally, we discuss how mesoscopic localization affects the response to structural interventions and how this framework could provide important insights for a broad range of dynamics.
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