None of the mutations currently documented in the novel coronavirus appear to make it more infectious, according to a study of virus genomes from over 15,000 COVID-19 patients from 75 countries.
The findings build on a study published in the journal Infection, Genetics and Evolution earlier this month which characterised patterns of diversity emerging in the genome of the SARS-CoV-2 virus that causes COVID-19.
"As a growing number of mutations have been documented, scientists are rapidly trying to find out if any of them could make the virus more infectious or deadly, as it's vital to understand such changes as early as possible," said Professor Francois Balloux from University College London (UCL) in the UK.
"We employed a novel technique to determine whether viruses with the new mutation are actually transmitted at a higher rate, and found that none of the candidate mutations appear to be benefiting the virus," said Balloux, lead author of the yet-to-be peer-reviewed study published as a pre-print on bioRxiv.
Coronaviruses, like other RNA viruses, 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 RNA modification systems which are part of host immunity, the researchers explained.
Most mutations are neutral, while others are advantageous or detrimental to the virus, they said. The scientists added that all these types of mutations can become more common as they get passed down to descendant viruses.
The team from UCL, and the University of Oxford in the UK, has so far identified 6,822 mutations in SARS-CoV-2 across the global dataset. The researchers said for 273 of the mutations, there is strong evidence that they have occurred repeatedly and independently.
Of those, they honed in on 31 mutations which have occurred at least 10 times independently during the course of the pandemic. To test if the mutations increase the transmission of the virus carrying them, the researchers modelled the virus's evolutionary tree.
They analysed whether a particular mutation was becoming increasingly common within a given branch of the evolutionary tree.
By doing this, the researchers tested whether, after a mutation first develops in a virus, descendants of that virus outperform their closely-related individuals that don't carry it.
The scientists found no evidence that any of the common mutations are increasing the virus's transmissibility. Instead, they found that some common mutations are neutral, but most are mildly detrimental to the virus.
The mutations analysed included one in the virus spike protein called D614G, which has been widely reported as being a common mutation which may make the virus more transmissible.
The new evidence finds that this mutation is in fact not associated with increased viral transmission.
The researchers found that 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.
"It is only to be expected that a virus will mutate and eventually diverge into different lineages as it becomes more common in human populations, but this does not necessarily imply that any lineages will emerge that are more transmissible or harmful," said Lucy van Dorp from UCL Genetics Institute.
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