Multiscale feedback drives viral evolution and epidemic dynamics

TL;DR

This paper presents a multiscale model linking within-host viral evolution to population-level epidemic dynamics, revealing how feedback mechanisms influence virus spread, evolution, and potential collapse scenarios.

Contribution

It introduces a minimal multiscale framework with explicit coupling between within-host viral dynamics and epidemiology, including a coarse-grained analysis of feedback effects.

Findings

Identification of a context-dependent error threshold influenced by epidemic prevalence.

Prediction of oscillatory dynamics arising from microscopic-macroscopic feedback.

Illustration of different viral strain behaviors, including replacement and self-limiting epidemics.

Abstract

We introduce a minimal multiscale framework that links within-host virus dynamics to population-level SIRS epidemiology through explicit, bidirectional coupling. At the microscopic layer, a two variant quasispecies (master and mutant genomes with packaged virions) evolves on a fast timescale. At the macroscopic layer, two infectious classes (master- and mutant-infected), susceptible, recovered, and deceased individuals evolve slowly. The two scales are connected through transmission rates that depend on instantaneous virion abundance and through prevalence-weighted effective replication rates. Exploiting the timescale separation, we formalize a coarse-grained slow-fast closure: the genome-virion subsystem rapidly relaxes to quasi-steady states that parameterize time-varying transmission in the slow epidemiological system. This yields an integrated expression for the basic reproduction number and sharp inequalities that delineate coexistence versus exclusion. A key prediction is a context-dependent error threshold that shifts with the prevalence ratio, enabling transient pseudo-error catastrophes driven by epidemic composition rather than intrinsic fidelity. Linearization reveals parameter regions with damped oscillations arising solely from the microscopic-macroscopic feedback. Two illustrative extremes bracket the model's behavior: an avirulent strongly immunizing strain that benignly replaces the master, and a hypervirulent weakly immunizing that self-limits via host depletion and collapses transmission. This framework yields testable signatures linking viral load, incidence, and within-host composition.