Societies change through time, entailing changes in behaviors and institutions. We ask how social change occurs when behaviors and institutions are interdependent. We model a group-structured society in which the transmission of individual behavior o
ccurs in parallel with the selection of group-level institutions. We consider a cooperative behavior that generates collective benefits for groups but does not spread between individuals on its own. Groups exhibit institutions that increase the diffusion of the behavior within the group, but also incur a group cost. Groups adopt institutions in proportion to their fitness. Finally, cooperative behavior may also spread globally. As expected, we find that cooperation and institutions are mutually reinforcing. But the model also generates behavioral source-sink dynamics when cooperation generated in institutional groups spreads to non-institutional groups, boosting their fitness. Consequently, the global diffusion of cooperation creates a pattern of institutional free-riding that limits the evolution of group-beneficial institutions. Our model suggests that, in a group-structured society, large-scale change in behavior and institutions (i.e. social change) can be best achieved when the two remain correlated, such as through the spread successful pilot programs.
Several biological and social contagion phenomena, such as superspreading events or social reinforcement, are the results of multi-body interactions, for which hypergraphs offer a natural mathematical description. In this paper, we develop a novel ma
thematical framework based on approximate master equations to study contagions on random hypergraphs with a heterogeneous structure, both in terms of group size (hyperedge cardinality) and of membership of nodes to groups (hyperdegree). The characterization of the inner dynamics of groups provides an accurate description of the contagion process, without losing the analytical tractability. Using a contagion model where multi-body interactions are mapped onto a nonlinear infection rate, our two main results show how large groups are influential, in the sense that they drive both the early spread of a contagion and its endemic state (i.e., its stationary state). First, we provide a detailed characterization of the phase transition, which can be continuous or discontinuous with a bistable regime, and derive analytical expressions for the critical and tricritical points. We find that large values of the third moment of the membership distribution suppress the emergence of a discontinuous phase transition. Furthermore, the combination of heterogeneous group sizes and nonlinear contagion facilitates the onset of a mesoscopic localization phase, where contagion is sustained only by the largest groups, thereby inhibiting bistability as well. Second, we formulate a simple problem of optimal seeding for hypergraph contagions to compare two strategies: tuning the allocation of seeds according to either node individual properties or according to group properties. We find that, when the contagion is sufficiently nonlinear, groups are more effective seeds of contagion than individual nodes.
The colocation of individuals in different environments is an important prerequisite for exposure to infectious diseases on a social network. Standard epidemic models fail to capture the potential complexity of this scenario by (1) neglecting the hig
her-order structure of contacts which typically occur through environments like workplaces, restaurants, and households; and by (2) assuming a linear relationship between the exposure to infected contacts and the risk of infection. Here, we leverage a hypergraph model to embrace the heterogeneity of environments and the heterogeneity of individual participation in these environments. We find that combining heterogeneous exposure with the concept of minimal infective dose induces a universal nonlinear relationship between infected contacts and infection risk. Under nonlinear infection kernels, conventional epidemic wisdom breaks down with the emergence of discontinuous transitions, super-exponential spread, and hysteresis.
Mathematical disease modelling has long operated under the assumption that any one infectious disease is caused by one transmissible pathogen spreading among a population. This paradigm has been useful in simplifying the biological reality of epidemi
cs and has allowed the modelling community to focus on the complexity of other factors such as population structure and interventions. However, there is an increasing amount of evidence that the strain diversity of pathogens, and their interplay with the host immune system, can play a large role in shaping the dynamics of epidemics. Here, we introduce a disease model with an underlying genotype network to account for two important mechanisms. One, the disease can mutate along network pathways as it spreads in a host population. Two, the genotype network allows us to define a genetic distance across strains and therefore to model the transcendence of immunity often observed in real world pathogens. We study the emergence of epidemics in this model, through its epidemic phase transitions, and highlight the role of the genotype network in driving cyclicity of diseases, large scale fluctuations, sequential epidemic transitions, as well as localization around specific strains of the associated pathogen. More generally, our model illustrates the richness of behaviours that are possible even in well-mixed host populations once we consider strain diversity and go beyond the one disease equals one pathogen paradigm.
Small disturbances can trigger functional breakdowns in complex systems. A challenging task is to infer the structural cause of a disturbance in a networked system, soon enough to prevent a catastrophe. We present a graph neural network approach, bor
rowed from the deep learning paradigm, to infer structural perturbations from functional time series. We show our data-driven approach outperforms typical reconstruction methods while meeting the accuracy of Bayesian inference. We validate the versatility and performance of our approach with epidemic spreading, population dynamics, and neural dynamics, on various network structures: random networks, scale-free networks, 25 real food-web systems, and the C. Elegans connectome. Moreover, we report that our approach is robust to data corruption. This work uncovers a practical avenue to study the resilience of real-world complex systems.
Several complex systems can be modeled as large networks in which the state of the nodes continuously evolves through interactions among neighboring nodes, forming a high-dimensional nonlinear dynamical system. One of the main challenges of Network S
cience consists in predicting the impact of network topology and dynamics on the evolution of the states and, especially, on the emergence of collective phenomena, such as synchronization. We address this problem by proposing a Dynamics Approximate Reduction Technique (DART) that maps high-dimensional (complete) dynamics unto low-dimensional (reduced) dynamics while preserving the most salient features, both topological and dynamical, of the original system. DART generalizes recent approaches for dimension reduction by allowing the treatment of complex-valued dynamical variables, heterogeneities in the intrinsic properties of the nodes as well as modular networks with strongly interacting communities. Most importantly, we identify three major reduction procedures whose relative accuracy depends on whether the evolution of the states is mainly determined by the intrinsic dynamics, the degree sequence, or the adjacency matrix. We use phase synchronization of oscillator networks as a benchmark for our threefold method. We successfully predict the synchronization curves for three phase dynamics (Winfree, Kuramoto, theta) on the stochastic block model. Moreover, we obtain the bifurcations of the Kuramoto-Sakaguchi model on the mean stochastic block model with asymmetric blocks and we show numerically the existence of periphery chimera state on the two-star graph. This allows us to highlight the critical role played by the asymmetry of community sizes on the existence of chimera states. Finally, we systematically recover well-known analytical results on explosive synchronization by using DART for the Kuramoto-Sakaguchi model on the star graph.
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 desc
ribed 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.
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 gather
ings. 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.
One can often make inferences about a growing network from its current state alone. For example, it is generally possible to determine how a network changed over time or pick among plausible mechanisms explaining its growth. In practice, however, the
extent to which such problems can be solved is limited by existing techniques, which are often inexact, inefficient, or both. In this article we derive exact and efficient inference methods for growing trees and demonstrate them in a series of applications: network interpolation, history reconstruction, model fitting, and model selection.
Mesoscopic pattern extraction (MPE) is the problem of finding a partition of the nodes of a complex network that maximizes some objective function. Many well-known network inference problems fall in this category, including, for instance, community d
etection, core-periphery identification, and imperfect graph coloring. In this paper, we show that the most popular algorithms designed to solve MPE problems can in fact be understood as special cases of the maximum likelihood formulation of the stochastic block model (SBM), or one of its direct generalizations. These equivalence relations show that the SBM is nearly universal with respect to MPE problems.
