Researchers have discovered that coronaviruses, such as SARS-CoV-2, possess certain genes that are crucial for their survival, even if they don’t produce functional proteins. Their research on the evolution of these unknown genes could aid in predicting which variants may pose greater risks.
Viruses are streamlined entities designed for infection. Their genetic material is quite small, often consisting of just a few critical genes, and they quickly discard unnecessary genomic material.
Typically.
Coronaviruses, including SARS-CoV-2 (the agent behind COVID-19), seem to challenge this norm at first glance. They include additional “accessory” genes beyond the minimum gene set needed for viral function, and the purpose of most of these extra genes remains unclear. However, researchers suspect these genes must have some essential role, or else they would have been phased out as the viruses evolved.
Recent findings from researchers at the University of Utah Health reveal that some of these viral genes have persisted despite not producing a functional protein, which is usually the primary role of most genes. Their exploration of how and why these enigmatic genes evolve could enhance predictions regarding the potential danger of specific viral variants.
“Viruses typically discard genes that are not beneficial in some way,” explains Stephen Goldstein, PhD, a postdoctoral researcher in human genetics at the Spencer Fox Eccles School of Medicine, University of Utah, and the study’s lead author. “So, what evolutionary factors influence which viral genes are retained and which are expelled?”
In an effort to clarify the role of these extra viral genes, Goldstein observed the evolution of accessory genes in real time using a mouse coronavirus. He was intrigued to find that one of the genes remained in the genome across numerous virus generations, even though it no longer produced a protein.
A similar phenomenon seems to be true for SARS-CoV-2. The gene known as ORF8 exists in most strains of the virus, despite the fact that in some variants, the resulting protein is relatively small and likely nonfunctional.
The researchers theorize that these apparently nonfunctional genes might influence the activity of other viral genes significantly. When a different accessory gene was lost in the mouse virus, the behavior of other genes altered. The team is currently examining the structure of this first accessory gene to determine its potential regulatory impact on other genes.
Goldstein notes that these discoveries highlight the need to look beyond just the protein that a gene produces when assessing the potential risks of viral variants. “The genetic sequence’s inherent function—not solely the protein’s role—could influence viral fitness and transmission over time,” he asserts. “There is another layer of evolution happening beneath the surface that we still have much to learn about.”
The findings were published in Current Biology under the title “Hidden evolutionary constraints dictate the retention of coronavirus accessory genes.”
