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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.
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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.
We study the evolutionary Prisoners Dilemma on two social networks obtained from actual relational data. We find very different cooperation levels on each of them that can not be easily understood in terms of global statistical properties of both networks. We claim that the result can be understood at the mesoscopic scale, by studying the community structure of the networks. We explain the dependence of the cooperation level on the temptation parameter in terms of the internal structure of the communities and their interconnections. We then test our results on community-structured, specifically designed artificial networks, finding perfect agreement with the observations in the real networks. Our results support the conclusion that studies of evolutionary games on model networks and their interpretation in terms of global properties may not be sufficient to study specific, real social systems. In addition, the community perspective may be helpful to interpret the origin and behavior of existing networks as well as to design structures that show resilient cooperative behavior.
Epidemic propagation on complex networks has been widely investigated, mostly with invariant parameters. However, the process of epidemic propagation is not always constant. Epidemics can be affected by various perturbations, and may bounce back to its original state, which is considered resilient. Here, we study the resilience of epidemics on networks, by introducing a different infection rate ${lambda_{2}}$ during SIS (susceptible-infected-susceptible) epidemic propagation to model perturbations (control state), whereas the infection rate is ${lambda_{1}}$ in the rest of time. Through simulations and theoretical analysis, we find that even for ${lambda_{2}<lambda_{c}}$, epidemics eventually could bounce back if control duration is below a threshold. This critical control time for epidemic resilience, i.e., ${cd_{max}}$ can be predicted by the diameter (${d}$) of the underlying network, with the quantitative relation ${cd_{max}sim d^{alpha}}$. Our findings can help to design a better mitigation strategy for epidemics.
Investigation of eigenvector localization properties of complex networks is not only important for gaining insight into fundamental network problems such as network centrality measure, spectral partitioning, development of approximation algorithms, but also is crucial for understanding many real-world phenomena such as disease spreading, criticality in brain network dynamics. For a network, an eigenvector is said to be localized when most of its components take value near to zero, with a few components taking very high values. In this article, we devise a methodology to construct a principal eigenvector (PEV) localized network from a given input network. The methodology relies on adding a small component having a wheel graph to the given input network. By extensive numerical simulation and an analytical formulation based on the largest eigenvalue of the input network, we compute the size of the wheel graph required to localize the PEV of the combined network. Using the susceptible-infected-susceptible model, we demonstrate the success of this method for various models and real-world networks consider as input networks. We show that on such PEV localized networks, the disease gets localized within a small region of the network structure before the outbreaks. The study is relevant in controlling spreading processes on complex systems represented by networks.
The size that an epidemic can reach, measured in terms of the number of fatalities, is an extremely relevant quantity. It has been recently claimed [Cirillo & Taleb, Nature Physics 2020] that the size distribution of major epidemics in human history is extremely fat-tailed, i.e., asymptotically a power law, which has important consequences for risk management. Reanalyzing this data, we find that, although the fatality distribution may be compatible with a power-law tail, these results are not conclusive, and other distributions, not fat-tailed, could explain the data equally well. As an example, simulation of a log-normally distributed random variable provides synthetic data whose statistics are undistinguishable from the statistics of the empirical data. Theoretical reasons justifying a power-law tail as well as limitations in the current data are also discussed.
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