Feng Qu, PhD
Professor
The Ohio State University
Wooster, Ohio, United States
Camila Perdoncini Carvalho
The Ohio State University
Wooster, Ohio, United States
Deya Wang
The Ohio State University
Wooster, Ohio, United States
Junping Han
The Ohio State University
Wooster, Ohio, United States
Khwannarin Khemsom (she/her/hers)
Graduate Student
The Ohio State University
Wooster, Ohio, United States
Viruses constantly evolve by enriching mutations that promote their survival and reproduction in changing environments. Understanding how such mutations become enriched promises to inform more effective strategies for controlling virus diseases of plants and animals. We previously identified a naturally occurring mutation of turnip crinkle virus (TCV), designated A113V, that altered a single amino acid (aa) residue of TCV p28/p88 replicase proteins. Here we report that this mutation specifically diminished the accumulation of sgRNA1, one of the two TCV subgenomic RNAs, and caused substantial delays in TCV systemic spread. Nevertheless, we were able to isolate multiple second-site mutations that restored sgRNA1 accumulation, and normal systemic spread, within six weeks of plant infections. The rapid emergence of compensatory mutations is consistent with the Bottleneck, Isolate, Amplify, Select (BIAS) hypothesis first proposed by us, which posits that viral mutations ascend to dominance through a series of intracellular reproductive population bottlenecks. Untangling these viral evolution mechanisms is expected to inspire more effective approaches for controlling virus diseases of plants, animals, and humans.