2026/01/27 by Anonymous, Juan C. Muñoz-Sánchez, J. Tomás Lázaro +2
Biochemistry, Genetics and Molecular Biology · Environmental Science · Mathematics · #Evolution and Genetic Dynamics #Bacteriophages and microbial interactions #COVID-19 epidemiological studies
paper · pdf · doi:10.1103/1533-5v14
We introduce a minimal multiscale framework that links within-host virus dynamics to population-level susceptible-infectious-recovered-susceptible (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 quasisteady states that parametrize 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 strain that self-limits via host depletion and collapses transmission. This framework yields testable signatures linking viral load, incidence, and within-host composition.