Coronavirus is NOT mutating to become more virulent: Scientific review suggests a vaccine is likely to work while debunking the myth the virus was created in a Chinese lab
- Study traced the evolutionary origins of the coronavirus back to its origin
- Found it is too different to other coronaviruses to have been man-made
- The virus has an unusually slow mutation rate and is not changing to become more severe or infectious
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