NEW YORK – An analysis of SARS-CoV-2 virus genomes obtained from more than 46,000 people with COVID-19 has shown that reccurent mutations in the virus do not appear to increase its transmission.
A team led by researchers at University College London published the findings in Nature Communications on Wednesday. Lucy van Dorp, a senior research fellow at the UCL Genetics Institute and first author on the paper, said the scientists embarked on the effort to make sense of the staggering number of SARS-CoV-2 genomes being generated around the world.
"We needed new approaches to analyze enormous amounts of data in close to real time to flag new mutations in the virus that could affect its transmission or symptom severity," van Dorp said in a statement. "Fortunately, we found that none of these mutations are making COVID-19 spread more rapidly."
However, she cautioned that the scientific community remain vigilant and continue to monitor new mutations, especially as vaccines for the virus are being introduced.
The research team involved with the study included UCL Genetics Institute, the University of Oxford, the French Agricultural Research Centre for International Development (Cirad), and the University of Reunion Island.
They analyzed virus genomes from 46,723 people with COVID-19, collected through July 2020 and obtained via the Global Initiative on Sharing All Influenza Data (GISAID). The samples came from individuals from 99 countries in all major continental regions.
From that data set, the researchers identified 12,706 viral mutations in the virus. Of these, just 398 appeared to have occurred repeatedly. They also flagged a subset of 185 mutations that have arisen at least three times independently during the pandemic. The scientists then modeled a phylogenetic tree and estimated whether viruses with these mutations were outperforming others.
They determined that most common mutations are neutral for the virus, including a spike protein mutation called D614G that a study appearing earlier this year in Cell had suggested was increasing transmission.
"We do not identify a single recurrent mutation in this set convincingly associated with increased viral transmission," the authors wrote.
As part of the study, the researchers also determined that most of the SARS-CoV-2 mutations were induced by the human immune system via RNA editing, rather than being viral adaptations. Still, they noted that the virus might have already developed mutations favoring transmission at an earlier stage in development, prior to the collection of the first genomes early in the outbreak in December of 2019.
"The virus seems well adapted to transmission among humans, and it may have already reached its fitness optimum in the human host by the time it was identified as a novel virus," van Dorp said.
Given the framework they developed, the researchers also said they will be able to track new mutations, which will likely occur in response to vaccines as they are being rolled out.
"The virus may well acquire vaccine-escape mutations in the future," said Francois Balloux, director of UCL Genetics and an author on the paper, "but we're confident we'll be able to flag them up promptly, which would allow updating the vaccines in time if required."