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Register a new userMaster equation analysis of mesoscopic localization in contagion dynamics on higher-order networks
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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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Recommendations around epidemics tend to focus on individual behaviors, with much less efforts attempting to guide event cancellations and other collective behaviors since most models lack the higher-order structure necessary to describe large gatherings. Through a higher-order description of contagions on networks, we model the impact of a blanket cancellation of events larger than a critical size and find that epidemics can suddenly collapse when interventions operate over groups of individuals rather than at the level of individuals. We relate this phenomenon to the onset of mesoscopic localization, where contagions concentrate around dominant groups.
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.
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.
In many real-world networks, the rates of node and link addition are time dependent. This observation motivates the definition of accelerating networks. There has been relatively little investigation of accelerating networks and previous efforts at analyzing their degree distributions have employed mean-field techniques. By contrast, we show that it is possible to apply a master-equation approach to such network development. We provide full time-dependent expressions for the evolution of the degree distributions for the canonical situations of random and preferential attachment in networks undergoing constant acceleration. These results are in excellent agreement with results obtained from simulations. We note that a growing, non-equilibrium network undergoing constant acceleration with random attachment is equivalent to a classical random graph, bridging the gap between non-equilibrium and classical equilibrium networks.
We explore simple models aimed at the study of social contagion, in which contagion proceeds through two stages. When coupled with demographic turnover, we show that two-stage contagion leads to nonlinear phenomena which are not present in the basic `classical models of mathematical epidemiology. These include: bistability, critical transitions, endogenous oscillations, and excitability, suggesting that contagion models with stages could account for some aspects of the complex dynamics encountered in social life. These phenomena, and the bifurcations involved, are studied by a combination of analytical and numerical means.
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