Lag-Induced Critical Transitions to Extinction in Replicating Systems

TL;DR

This paper reveals how explicit delays in replication timing can cause critical transitions to extinction in replicating systems, offering new insights into antiviral strategies and the dynamics of population collapse.

Contribution

It introduces the concept of lag-induced critical transitions in replicating systems, highlighting the role of replication timing delays as an independent control parameter for extinction.

Findings

Delay in replication timing can induce extinction independently of mutation rates.

Replication timing acts as a control parameter influencing system stability.

Modulating replicase availability offers potential antiviral strategies.

Abstract

Replicating systems sustained by error-prone enzymatic amplification can undergo critical transitions between persistence and extinction. In RNA viruses, such transitions are classically governed by mutation rates and fitness landscapes, giving rise to error thresholds and lethal mutagenesis. Motivated by experimental evidence that polymerase-targeting antivirals constrain replication, we analyze replicating systems with explicit delays in replication-enzyme availability. We identify a lag-induced (dynamical) critical transition driven by the loss of temporal coordination between genome translation and replication. At a fixed mutation rate and replicative fitness landscape, populations cross an extinction threshold solely due to time delays. Within the quasispecies framework, replication-translation timing emerges as an independent control parameter, defining a distinct dynamical route to extinction and suggesting new antiviral strategies based on modulating replicase availability. More generally, we propose that the pathway to collapse described in this article can be understood as lag-time-induced tipping (\tau-tipping).