Extinction pathways in dengue-Zika multi-pathogen systems with antibody-dependent enhancement

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Introduction Antibody-dependent enhancement (ADE) creates complex multi-pathogen dynamics that fundamentally alter extinction probabilities in co-circulating dengue and Zika viruses. Methods We develop a stochastic framework for five co-circulating pathogens (dengue serotypes 1 -4 and Zika) with asymmetric ADE. Using WKB large-deviation theory, we compute extinction actions and most-probable pathways via Minimum Action, Nudged Elastic Band, and adaptive SVD methods. WKB actions are validated against Monte Carlo simulations (Pearson r = 0.98, max relative error 0.3%). Results The model predicts that DENV4 acts as a keystone pathogen: its elimination triggers a cascade (DENV4 → DENV2 → Zika) that is exponentially more probable than direct multi-pathogen extinction. The parameter space separates into three extinction regimes –sequential, pairwise, and total collapse –with hysteresis near η≈2.8 Sensitivity analysis shows keystone identity is stable under ±20% ADE matrix perturbations. In a symmetric n-pathogen limit on the symmetric invariant manifold, single-serotype extinction action decreases as 1/n while global elimination action grows as n ·𝒮 sym . Discussion Within this symmetric idealization, this provides a possible mechanistic reference point for understanding how serotype diversity could simultaneously promote local vulnerability and global persistence. Whether a similar relationship holds in the fully asymmetric dengue-Zika system is an open question. Limitations include the direct-transmission approximation (quantitative error < 15%) and time-averaged ADE. All predictions are model-based and require empirical validation.

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