Coronavirus mutations provide insight into spread patterns

An international research team has discovered nearly 200 recurrent mutations in the genome of SARS-CoV-2, the virus that causes COVID-19 disease. 

The team, led by scientists at the Genetics Institute at University College London, analysed 7666 viral genomes from coronavirus patients across the globe which had been made available on an open-source platform. 

'All viruses naturally mutate,' said study senior author Professor Francois Balloux. 'So far we cannot say whether SARS-CoV-2 is becoming more or less lethal and contagious.'

The team analysed the genomes for genetic variability and found 198 recurring mutations, many of which appear to have emerged more than once in different strains. As the virus has only recently started to infect humans, this could be a sign of adaptation to the novel host but is not necessarily a reason to worry. 

'The vast majority of mutations observed so far in SARS-CoV-2 circulating in humans are likely neutral' with no effect on its virulence or fatality rate, the authors said. 

The team calculated an average mutation rate for SARS-CoV-2 and determined it was largely comparable to other RNA viruses in circulation. This mutation rate allowed the scientists to determine that the virus first infected humans between 6 October and 11 December 2019.

This contradicts speculation that the virus had been circulating in the population long before being characterised, which could have meant a larger percentage of people might have already contracted it and possibly become immune. 

'Everyone was hoping for that,' Professor Balloux told CNN. 'I was too.' 

Other controversial, or non peer-reviewed publications have suggested that the virus evolved into distinct subgroups in different countries, but this research indicates there was 'no evidence for the evolution of distinct phenotypes in SARS-CoV-2 at this stage'. The paper concluded that in many countries – including the UK – the diversity of viral genomes was comparable, indicating that the virus entered the UK numerous times independently, rather than via a single case.

Interestingly, the mutations observed were not evenly distributed across the viral genome. Scientists hope that the areas with very few mutations could be viable targets for drug and vaccine development. 

'A major challenge to defeating viruses is that a vaccine or drug might no longer be effective if the virus has mutated. If we focus our efforts on parts of the virus that are less likely to mutate, we have a better chance of developing drugs that will be effective in the long run.' Professor Balloux said.