ArXiv TLDR

Scale-dependent Temporal Signatures of Arboviral Transmission in Urban Environments

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2604.11818

Marcílio Ferreira dos Santos, Cleiton de Lima Ricardo

q-bio.PEmath.PR

TLDR

A new spatiotemporal model reveals that arboviral epidemic differentiation in urban areas is scale-dependent, primarily driven by temporal dynamics, not spatial proximity.

Key contributions

  • Proposes a probabilistic spatiotemporal framework for analyzing arboviral transmission.
  • Finds spatial proximity is not discriminatory for disease differentiation at the urban scale.
  • Shows epidemic differentiation emerges only beyond a critical temporal window.
  • Highlights the importance of biologically grounded and scale-aware epidemic modeling.

Why it matters

This paper challenges conventional wisdom by showing that spatial proximity is less critical than temporal scale in differentiating arboviral epidemics in cities. It underscores the need for more sophisticated, biologically informed models to accurately understand and predict disease spread, offering a new perspective for public health interventions.

Original Abstract

Understanding epidemic dynamics in urban environments requires models that capture interactions across space and time while incorporating biological constraints. In this work, we propose a probabilistic spatiotemporal framework based on pairwise interaction kernels to analyze arboviral transmission using large-scale georeferenced data from Recife, Brazil. The model describes interactions as a function of spatial distance and temporally delayed influence, with parameters estimated via maximum likelihood. Our results reveal a marked asymmetry between spatial and temporal components. The spatial parameter systematically collapses, indicating that spatial proximity does not provide discriminatory information between diseases at the urban scale. In contrast, temporal dynamics exhibit scale-dependent behavior: statistical differentiation between dengue, Zika, and chikungunya emerges only beyond a critical temporal window. We show that unconstrained models primarily capture short-term co-occurrence, leading to apparent but non-robust differences, while biologically constrained models reveal a common underlying transmission structure. Additionally, reconstructed transmission networks exhibit localized and structured interaction patterns consistent with plausible epidemic propagation. These findings demonstrate that epidemic differentiation is not intrinsic, but an emergent phenomenon dependent on temporal scale, highlighting the importance of biologically grounded and scale-aware modeling in spatiotemporal epidemic analysis.

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