SARS-CoV-2 is the virus that causes the illness COVID-19. In the mutation, 81 letters in the virus’s genome had been deleted.
Viral mutations are a normal part of a virus’s evolution and can alter the severity of the disease they cause.
In the case of SARS-CoV-2, the finding is of interest because the nature of the mutation suggests it may have an association with a less severe form of the disease. A less virulent virus may have a selective advantage over other strains.
The research, by a team of scientists at the Arizona State University (ASU), United States, is now a correspondence piece in the Journal of Virology.
While some researchers have focused much attention on tracking the number of cases of COVID-19 against the global spread of SARS-CoV-2, others are tracking the virus as it begins to mutate, creating changes in its genetic code that may affect how it functions.
Mutations occur when a change in genetic material incorporates in the viral genome and passes on to the following generation. In the case of viruses, a generation is usually the cycle of infection of a particular cell.
The team from ASU was originally doing research on influenza viruses, analyzing nasal swab samples it took from participants in Arizona.
However, once health authorities started confirming COVID-19 cases in Arizona, the team decided to switch their research to focus on SARS-CoV-2.
According to Dr. Efrem Lim, an assistant professor in the School of Life Sciences at ASU and lead of the research team, “[t]his was the scientific opportunity of a lifetime for ASU to be able to contribute to understand how this virus is spreading in our community. As a team, we knew we could make a significant difference.”
After removing the influenza nasal swabs from their study, the team had 382 samples left. Of these, they confirmed that five contained SARS-CoV-2.
The team then conducted next generation sequencing on the RNA of the SARS-CoV-2 samples, which allowed them to quickly determine the 30,000 characters of the virus’s genetic code.
After comparing these to sequences of SARS-CoV-2 deposited in the nonprofit GISAID’s EpiCoVTM Database, it became clear that one of the viruses had a unique mutation that involved the deletion of 81 letters from its genome.
For Dr. Lim, “[o]ne of the reasons why this mutation is of interest is because it mirrors a large deletion that arose in the 2003 SARS outbreak.”
Previous research has suggested that similar deletions reduced the ability of the coronavirus at the heart of the 2003 SARS outbreak to replicate. A weakened virus may have a reduced short-term selective advantage — but it may have an increased selective advantage in the mid to long term.
The deletions that the ASU team identified in SARS-CoV-2 affect parts of the code that produce a particular protein. The scientists believe that this protein is key to helping SARS-CoV-2 evade human defenses, allowing it to replicate quickly.
The mutation in the virus may be valuable in helping scientists better understand how SARS-CoV-2 makes people ill. Similarly, it may help in the development of antiviral drugs that can reduce the severity of the disease until an effective vaccine comes along.
However, scientists need to do more research first. The team at ASU is currently exploring precisely what effect the mutation has on the way the virus functions.
The researchers have also joined up with the Translational Genomics Research Institute, the University of Arizona, and Northern Arizona University to create the Arizona COVID-19 Genomics Union, which intends to study SARS-CoV-2 mutations further.
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