The mutations currently documented in the novel coronavirus which causes COVID-19 do not appear to increase its transmissibility in humans, according to a study that analyzed samples of the virus from more than 46,000 individuals across the world.
The research, published in the journal Nature Communications, analysed a global dataset of virus genomes from 46,723 people with COVID-19 from 99 countries, collected up until the end of July 2020.
“We realised early on in the pandemic that we needed new approaches to analyse enormous amounts of data in close to real time to flag new mutations in the virus that could affect its transmission or symptom severity,” said study corresponding author Lucy van Dorp from the University College London in the UK.
“Fortunately, we found that none of these mutations are making COVID-19 spread more rapidly, but we need to remain vigilant and continue monitoring new mutations, particularly as vaccines get rolled out,” van Dorp said.
According to the researchers, coronaviruses like SARS-CoV-2 can develop mutations in three different ways — by mistake from copying errors during viral replication, through interactions with other viruses infecting the same cell, or they can be induced by the host’s immune system.
While most mutations are neutral, they said others can be advantageous or detrimental to the virus, adding that both can become more common as they get passed down to descendant viruses.
In the current research, the scientists identified 12,706 mutations in SARS-CoV-2 of which 398 had strong evidence that they occurred repeatedly and independently.
The researchers then honed in on 185 of the 398 mutations which occurred at least three times independently during the course of the pandemic.
They modelled the virus’ evolutionary tree, and analysed whether, after a mutation first develops in a virus, its descendants outperform closely-related variants without that particular mutation.
According to the study, there was no evidence that any of the common mutations are increasing the virus’ transmissibility.
On the contrary, the scientists found that most common mutations are neutral for the virus.
This includes one mutation in the virus spike protein called D614G, which has been widely reported as being a common mutation that may make the virus more transmissible, they added.
Most of the common mutations appear to have been induced by the human immune system, rather than being the result of the virus adapting to its novel human host, the scientists said.
“We previously estimated SARS-CoV-2 jumped into humans in October or November 2019, but the first genomes we have date to the very end of December,” said study lead author Francois Balloux from UCL.
“By that time, viral mutations crucial for the transmissibility in humans may have emerged and become fixed, precluding us from studying them,” Balloux said.
The scientists said a virus mutates and eventually diverges into different lineages as it becomes more common in human populations.
However, this does not necessarily imply that any lineages will emerge that are more transmissible or harmful, they added.
“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 added.
The researchers believe the imminent introduction of vaccines is likely to exert new selective pressures on the virus to escape recognition by the human immune system.
They cautioned that his may lead to the emergence of vaccine-escape mutants which they said could be identified using their computational framework.
“The news on the vaccine front looks great. The virus may well acquire vaccine-escape mutations in the future, but we’re confident we’ll be able to flag them up promptly, which would allow updating the vaccines in time if required,” Balloux concluded.
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