We know that the coronavirus behind the COVID-19 crisis lived harmlessly on bats and other wildlife before it jumped over the species barrier and spread to humans.
Researchers at Duke University have now identified a number of “silent” mutations in about 30,000 characters of the virus. Genetic code It helped prosper after the leap and probably set the stage for a pandemic. Subtle changes included how the virus folds its RNA molecule inside human cells.
Published in the journal on October 16th for research PeerJ, Researcher used Statistical method They were developed to identify adaptive changes in the human SARS-CoV-2 genome, rather than the closely associated coronavirus found in bats and pangolins.
“We’re trying to figure out why this virus is so unique,” said Alejandro Berrio, a postdoctoral fellow in the lab of biologist Gregory Ray at Duke University.
Previous studies have detected positive selection fingerprints in genes encoding “spike” proteins scattered on the surface of the coronavirus. It plays an important role in the ability to infect new cells.
New studies also flag mutations that alter spike proteins, suggesting that viral strains carrying these mutations are likely to thrive. However, with their approach, research authors Verio, Ray, and Duke also identified additional causes that student Valerie Gartner could not detect in previous studies.
Researchers have found that two other regions of the SARS-CoV-2 genome, so-called silent mutations called Nsp4 and Nsp16, have a biological advantage over the virus over previous strains without altering the encoding protein. It is reported that it seems to have given.
Instead of affecting proteins, Verio said it’s likely that the genetic material of the virus, made up of RNA, affected how it folds into 3D shapes and functions in human cells.
According to Verio, it is not yet known what these changes in RNA structure did to distinguish the human SARS-CoV-2 virus from other coronaviruses. However, they may have contributed to the ability of the virus to spread before people realize that they have it. This is a significant difference that is far more difficult to control the current situation than the 2003 SARS coronavirus outbreak.
The study could lead to new molecular targets for the treatment or prevention of COVID-19, Verio said.
“Nsp4 and Nsp16 are one of the first RNA molecules to be produced when: Virus It infects new people, “Berio said. protein It will not be expressed until later. Therefore, it appears early in the life cycle of the virus and can create better therapeutic targets. “
More generally, by identifying the genetic alterations that have allowed new coronaviruses to thrive in human hosts, scientists are better off developing future zoonotic diseases before they occur. I want to predict.
“The virus is constantly changing and evolving,” Verio said. “Therefore, like SARS-CoV-2, new strains of coronavirus that can infect other animals may emerge and spread to people. We recognize it and You need to work hard. Contain quickly. ”
A positive selection, independent of the effects of Alejandro Berrio et al, SARS-CoV-2 and other coronaviruses on protein function in the genome, PeerJ (2020). DOI: 10.7717 / peerj.10234
Duke University School of Nursing
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