SARS-CoV-2 variants of concern emerging from chronic COVID infections, study shows

[SWAlexander]

The coronavirus variants of concern are emerging from chronic, long-term COVID infections in people who may be immune comprised and unable to clear the virus, a new study strongly suggests. Frontiers in Virology published the findings by scientists at Emory University and the University of Oxford.

"Rather than evolving from transmission chains of acute COVID infections in hundreds of millions of people, our results show that the variants of concern come from rare cases when someone may have an active infection for months," says Daniel Weissman, a corresponding author and Emory professor of biology and physics focused on quantitative evolutionary theory.

Viruses like SARS-CoV-2 continuously evolve due to occasional mutations in the genetic code that may occur when they replicate. "When a virus copies itself, it doesn't always make perfect copies," Weissman explains.
https://www.news-medical.net/news/2...c-long-term-COVID-infections-study-shows.aspx

 

[Pyrrhus]

Thanks for sharing. Here's the actual (Ghafari et al., 2022) study:

Investigating the evolutionary origins of the first three SARS-CoV-2 variants of concern (Ghafari et al., 2022)
https://www.frontiersin.org/articles/10.3389/fviro.2022.942555/

Excerpt:

The emergence of Variants of Concern (VOCs) of SARS-CoV-2 with increased transmissibility, immune evasion properties, and virulence poses a great challenge to public health. Despite unprecedented efforts to increase genomic surveillance, fundamental facts about the evolutionary origins of VOCs remain largely unknown.

One major uncertainty is whether the VOCs evolved during transmission chains of many acute infections or during long-term infections within single individuals. We test the consistency of these two possible paths with the observed dynamics, focusing on the clustered emergence of the first three VOCs, Alpha, Beta, and Gamma, in late 2020, following a period of relative evolutionary stasis.

We consider a range of possible fitness landscapes, in which the VOC phenotypes could be the result of single mutations, multiple mutations that each contribute additively to increasing viral fitness, or epistatic interactions among multiple mutations that do not individually increase viral fitness—a “fitness plateau”.

Our results suggest that the timing and dynamics of the VOC emergence, together with the observed number of mutations in VOC lineages, are in best agreement with the VOC phenotype requiring multiple mutations and VOCs having evolved within single individuals with long-term infections.

(Spacing added for readability)