ArticleFrontiers in immunology2026
Heterogeneous immune recovery after viral response through a dynamical model of feedback-driven persistence and clearance.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- From IL-6 production to IL-6R buffering: a unified IL-6-IL-6R framework for immune homeostasis during viral infection.Frontiers in immunology · 2026Review
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4 authors.
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Abstract
Viral infections trigger complex immune responses with heterogeneous outcomes shaped by nonlinear feedback. A system of ordinary differential equations is developed to investigate immune response dynamics during viral infection, incorporating six modules, including viral load, innate immunity, cellular immunity, humoral immunity, immune suppression, and IL-6. Bifurcation analysis reveals that under continuous viral exposure, when viral clearance rate and intrinsic viral death rate satisfy specific conditions, the system exhibits up to five stable equilibria. This indicates that different health and disease states may coexist depending on initial conditions, while severe inflammation mainly arises from strong activation of cellular immunity, highlighting the complexity of immune responses. Simulations of finite-time viral exposure demonstrate multi-timescale recovery characteristics, with viral load and IL-6 levels declining rapidly, while humoral immune activation and immunosuppression show delayed and sustained patterns. Furthermore, analysis of infectious period and disease duration also indicates that during transition from early acute response to chronic disease, viral replication rate plays a critical role, while immune response intensity is sensitive to both viral clearance and immune self-activation. Subsystem analysis identifies the three-component subsystem of viral load, innate immunity, and cellular immunity as core drivers of bistability and oscillations, while humoral immunity, immune suppression, and IL-6 primarily modulate response amplitude and timing. This work establishes a theoretical framework for analyzing immune response and chronic risks through feedback dynamical modelling, providing insights for intervention strategies.
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