Mesoscale community organization governs epidemic onset and spread in metapopulations
Haoyang Qian, Malbor Asllani
TL;DR
The paper develops a two-scale framework for epidemic spreading in hierarchically structured metapopulations by embedding local contact networks within a diffusion-driven mobility layer. Using IBMF and a degree-based DBMF reduction, it derives an effective transmission rate tilde{β}_{μ} = β ⟨k⟩_{μ} / N and shows that internal community connectivity drives onset and spread, with stability analyzed via spectral perturbation theory. A key finding is that above-average-density metacommunities amplify transmission and skew spatial infection patterns, a result made concrete through second-order perturbation corrections and localization of Laplacian eigenvectors. The authors further demonstrate predictive power by linking the leading eigenvector of the Jacobian to the steady-state infection distribution and validating the approach against nine empirical mobility networks. Overall, the work provides a scalable, theory-grounded toolkit for vulnerability assessment and targeted interventions in structured populations, with implications for metaplex-inspired multiscale dynamics.
Abstract
Understanding how internal community structure shapes the course of epidemics remains a fundamental challenge in modeling real-world populations. Standard metapopulation models often assume uniform mixing within communities, overlooking how internal heterogeneity affects global outcomes. Here, we develop a general framework for epidemic spreading in hierarchically structured metapopulations, where individuals interact locally within dense communities and move across a broader network. We show that transmission dynamics are governed by the mesoscale organization of these communities: highly connected groups accelerate and amplify outbreaks, while less connected ones dampen spread. Through a combination of mean-field theory, spectral analysis, and stability methods, we reveal a direct link between internal connectivity and the emergence of uneven, spatially structured epidemic patterns. We further validate these predictions using real-world data, where social contact networks capture the local scale of transmission while spatial transport networks govern global connectivity, confirming the robustness of our framework across scales. These results demonstrate how community structure fundamentally governs the shape of epidemics in complex, networked populations, offering new insights into vulnerability, containment, and epidemic control.
