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From Trait-Structured Within-Host Dynamics to SIR Models: A Multiscale Framework With Re-Exposure.

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  • 1Department of Mathematics, University of British Columbia, Vancouver, BC, V6T 1Z2, Canada.

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Summary
This summary is machine-generated.

This study introduces a novel framework linking within-host infection dynamics to population-level models. It reveals how individual immune responses and pathogen inoculum size drive disease transitions and persistence, even below a basic reproduction number of one.

Keywords:
Immune thresholdsMultiscale SIR projectionRe-exposure dynamicsTrait-structured immunityWithin-host dynamics

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Area of Science:

  • Mathematical Biology
  • Epidemiology
  • Immunology

Background:

  • Understanding the link between within-host pathogen dynamics and population-level disease spread is crucial for effective public health strategies.
  • Existing multiscale models often use ad hoc linking functions, limiting their mechanistic consistency.
  • Heterogeneity in immune responses and pathogen inoculum size can significantly influence infection outcomes.

Purpose of the Study:

  • To develop a unified, threshold-based multiscale framework connecting within-host infection dynamics to a structured population model.
  • To derive population compartments directly from within-host trajectories, avoiding artificial linking mechanisms.
  • To investigate the impact of inoculum thresholds and immune activation on disease dynamics and epidemic indicators.

Main Methods:

  • Developed a two-variable within-host model for pathogen load and immune response, incorporating Allee-like inoculum thresholds and nonlinear immune activation.
  • Derived mapping rules to classify continuous within-host trajectories into susceptible, infected (low/high immune protection), and recovered states.
  • Formulated a next-generation operator for trait-structured re-exposure and an explicit R0 expression for global mixing scenarios.

Main Results:

  • Simulations demonstrated sharp transitions between pathogen clearance and persistence, influenced by inoculum size and immune status.
  • Observed an emergent cascade: susceptible -> infected (low immunity) -> infected (high immunity) -> recovered.
  • Chronic within-host equilibria sustained infection even when the basic reproduction number (R0) was less than 1, exhibiting backward-bifurcation-like population dynamics.

Conclusions:

  • The framework provides a consistent method to link immunological heterogeneity to epidemic indicators.
  • Identified potential for chronic infection reservoirs and backward-bifurcation phenomena driven by within-host dynamics.
  • Enables estimation of disease control thresholds directly from within-host measurements, improving dose-response data interpretation.