"Acute Infection as a Transient Destabilizer in Persistence-Based Systems"

This work presents a minimal dynamical systems framework for understanding how biological systems transition across the lifespan from plastic, open regimes to stabilized, closed regimes. The model formalizes the interaction between plasticity and stability as coupled variables, capturing how transient perturbations—particularly acute infections—can induce lasting, path-dependent changes in system behavior. Within this framework, restoration is regime-dependent: open systems realign with external inputs, whereas closed systems return to pre-existing attractor states. This leads to asymmetric restoration, where movement toward reduced plasticity occurs readily, but reopening requires targeted intervention. The model naturally produces hysteresis, explaining why recovery trajectories differ from the paths that produced dysfunction. The framework integrates observations from aging biology and systems immunology, including infection-driven immune remodeling, loss of repertoire diversity, and the persistence of maladaptive states following incomplete resolution. It generates testable predictions linking measurable biomarkers—such as transcriptional entropy and T-cell receptor diversity—to intervention timing and long-term outcomes. By unifying these phenomena under a simple dynamical structure, this work reframes biological aging and chronic disease as consequences of accumulated regime transitions driven by perturbation history. It provides a foundation for designing interventions that exploit transient windows of plasticity to reshape long-term system trajectories.