- Scientists from Duke University have found silent mutations in SARS-CoV-2
- These mutations, they say, have helped the virus thrive in human hosts
- They believe their findings may assist with treating or preventing Covid-19
Understanding the features of SARS-CoV-2, the virus that causes Covid-19, is crucial for predicting the future, and in a recent study, scientists may have come one step closer.
According to Duke University (DU) researchers, a number of “silent” mutations in the roughly 30 000 letters of the virus’s genetic code may have given it an advantage and caused it to thrive in the human population after crossing over from bats and other wild animals.
"We're trying to figure out what made this virus so unique," said lead author Alejandro Berrio, a postdoctoral associate in biologist Greg Wray's lab at DU.
In their paper, they explain how the subtle changes, or mutations, influenced how the virus unfolded its RNA molecules within human cells.
The study was published in the journal PeerJ.
For their study, the researchers wanted to identify adaptive changes that occurred in the SARS-CoV-2 genome in humans, but not in closely related coronaviruses found in bats and pangolins.
A previous Health24 article explains that each virus contains its own unique genome, and understanding it can help researchers understand more about that virus.
The researchers used statistical methods they developed to investigate these changes and flagged mutations that altered the spike proteins. The spike proteins act as a doorway and essentially allow the virus access to invade the host, in this case, human cells.
It is therefore possible, the researchers wrote, that the viral strains carrying these mutations were more likely to thrive.
Additional culprits: silent mutations
Most importantly, the team identified additional culprits that were previously undetected: so-called “silent” mutations in two other regions of the SARS-CoV-2 genome, named Nsp4 and Nsp16, which they believe have given the virus a biological advantage over previous coronavirus strains, without altering the proteins they encode.
Instead of affecting the proteins, Berrio explained that the changes likely affected how the virus’s RNA folds up into three-dimensional (3D) shapes and functions inside human cells.
Unfortunately, what these changes in RNA structure might have done to set the SARS-CoV-2 virus in humans apart from other coronaviruses is still unknown, said Berrio, although they may have contributed to the virus's ability to spread before people even know they have it (also known as asymptomatic cases).
These kinds of cases have made a significant difference to the pandemic as it has made it that much more difficult to control than the 2003 SARS coronavirus outbreak.
How the findings can be beneficial
The authors explained that their discovery could lead to new molecular targets for treating or preventing Covid-19.
"Nsp4 and Nsp16 are among the first RNA molecules that are produced when the virus infects a new person," said Berrio.
"The spike protein doesn't get expressed until later. So they could make a better therapeutic target because they appear earlier in the viral life cycle."
More than this, if scientists continue to understand the genetic changes that enabled SARS-CoV-2 to thrive in human hosts, they may also better predict future zoonotic disease outbreaks before they happen.
"Viruses are constantly mutating and evolving. So it's possible that a new strain of coronavirus capable of infecting other animals may come along that also has the potential to spread to people, like SARS-CoV-2 did.
“We'll need to be able to recognise it and make efforts to contain it early," commented Berrio.