Viral Evolution Under Physical Constraints: Decay, Mutation, and Transmission as a Constrained Optimization Problem

TL;DR

This work advances a hazard-based framework that treats viral evolution as constrained optimization over environmental decay, within-host replication under immune pressure, and mutation feasibility, unified by the total transmission fitness $\Phi = \frac{R}{\lambda}$. By modeling virions as multi-component systems with hazard rates, the authors show how structural complexity trades off against environmental persistence and immune modulation, producing emergent viral classes and seasonally driven patterns. The framework accounts for diverse strategies—from environmentally stable, mutation-rich pathogens to latency- or immune-modulation–driven transmitters—while highlighting fundamental limits on eradicability and long-term control. The approach offers a principled lens for interpreting viral diversity, guiding surveillance, and informing public health interventions that target the dominant hazard or timing bottlenecks.

Abstract

Viruses display striking diversity in structure, transmission mode, immune interaction, and evolutionary behavior. Despite this diversity, viral strategies are not unconstrained. Here we present a unifying framework that treats viral evolution as a problem of constrained optimization governed by physical decay, immune pressure, mutation robustness, and transmission architecture. We model virions as multi-component physical systems subject to irreversible environmental failure and viruses as replicators operating under immune-driven selection and mutation-selection balance. Within this framework, major viral transmission strategies arise as necessary solutions rather than taxonomic accidents. Environmentally transmitted and airborne viruses are predicted to be structurally simple, chemically stable, and reliant on replication volume rather than immune suppression. Structurally complex viruses tolerate rapid environmental decay by encoding immune-modulatory machinery, latency, or persistent replication, at the cost of reduced mutation robustness. Temperature-dependent seasonality emerges naturally from the thermally activated nature of viral decay, without invoking host behavior.