The virus which causes Covid-19, called SARS-CoV-2, is mutating at an unusually slow rate, a new study finds.
Analysis by experts at the Royal Society also found none of the alterations made so far to the coronavirus’s genetic code are making it more infectious or severe.
The findings are reassuring for clinicians and epidemiologists as it indicates people who have previously caught the disease will have protection from reinfection.
It also offers hope that, when a vaccine is available, it will be effective in the long term.
Other findings from the study prove the coronavirus evolved naturally in bats and was not forged in a Chinese lab, as some conspiracy theories claim.
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Analysis by experts at the Royal Society found none of the alterations to the coronavirus’s genetic code are making it more infectious or severe. Other findings from the study prove the coronavirus evolved naturally in bats and was definitely not forged in a Chinese lab
A rapid review of available data has been published as a pre-print by the Royal Society’s SET-C (Science in Emergencies Tasking – COVID-19) task force, made up of Britain’s leading virologists.
They say the location and nature of mutations on SARS-CoV-2 have thus far not impacted its virulence.
It had previously been suggested by experts that the virus was mutating and becoming less severe but more infectious.
Now, according to the latest findings, this theory can be comprehensively dispelled.
The mutations that have evolved so far throughout the pandemic have instead left markers that allows researchers to track the spread of the virus.
This is a key tool in allowing policy makers to decide how best to restrict the spread of the contagion.
Professor Geoffrey Smith, the lead author of the research at the department of pathology at the University of Cambridge, said: ‘It is good news that SARS-CoV-2 has so far proven pretty stable, because it is easier to detect and treat a virus that is fairly stationary.
‘Whole genome sequencing allows us to understand not just that someone is infected, but to define precisely the strain of virus and so work out where the infection probably came from.
‘It also allows us to track strains of virus that become dominant and that might replicate or transmit more efficiently.’
One downside that the researchers point out is that even a slow mutation rate could allow the virus to develop resistance to certain drugs.
But these are speculative issues and, in the virus’s current guise, the authors of the study are confident the disease is not becoming more severe or infectious.
SARS-CoV-2, the virus which leads to Covid-19, has a protein on its surface which binds to a receptor on human cells called ACE2 and this is how it invades the body
How one amino acid led to a major mutation
The study by the Royal Society’s SET-C (Science in Emergencies Tasking – COVID-19) task force also studied the one major mutation SARS-CoV-2 underwent.
It is located on the S-protein which sticks out from the surface of the virus.
This spike latches on to the ACE2 receptor of human cells, tricks it into opening the cell, and allows the pathogen to infect a person.
At one specific location — residue 614 on the S1 terminus — the original form of the coronavirus had the amino acid aspartate, labelled with a D.
However, a random mutation saw this amino acid replaced with a glycine, labelled with a G.
The so-called D614G mutation was seen in barely any samples taken in February.
However, by March, more than a quarter (26 per cent) of isolated SARS-CoV-2 strains contained the mutation.
By May this figure had reached 70 per cent.
The D614G mutation i the most dominant one seen globally.
This mutation appears to help more virus infect a person and for more efficient infection of cells.
The D614G virus is also almost always accompanied with three other minor mutations. The role of these changes remains unknown.
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As part of the study, the experts looked at the origin of the virus in the UK and traced it back to its genetic origin.
They found its closest relative is a bat coronavirus found in China called RaTG13.
However, it is only 97 per cent identical – an enormous difference when it comes to viral genetic material.
Previous research found that it is possible SARS-CoV-2 first split from its ancestor in 1948 and has been residing in bats, who are immune, for around 70 years.
According to the experts, the difference between SARS-CoV-2 and other coronaviruses is too large for it to have been made in a lab and deliberately released.
‘The degree of divergence between SARS-CoV-2 and all other known coronaviruses is sufficient to refute the assertion that the COVID-19 pandemic arose by the deliberate or accidental release of a known virus (e.g. RaTG13) and makes the unsupported claim that SARS-CoV-2 was created artificially in a laboratory highly improbable,’ the researchers explain in their paper.
Instead, the study confirms the virus jumped into humans either straight from bats or via an intermediary mammalian host.
Professor Smith said: ‘There is nothing like solid evidence to bust the myths that are spread by conspiracy theorists.
‘It is understandable that when a new virus emerges there will be speculation about its origins, but the pace at which the global science community has developed our understanding of the genetics of SARS-CoV-2 has been spectacular.
‘That has allowed us to trace its spread and develop diagnostic tests and candidate vaccines.
‘It also allows us to debunk some of the more colourful conspiracy theories.’
In the process of coming to this conclusion the authors, who are some of the UK’s foremost experts, found that between February and March 2020, a total of 1,356 genetically distinct SARS-CoV-2 strains were brought into the UK from abroad.
More than a third (34 per cent) came from Spain, which was an early epicentre of the outbreak, while 14 per cent came from Italy, another major hotspot in the early days of the pandemic.
Twenty-nine per cent stemmed from France, while less than one per cent derived from travel between the UK and China.
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