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.”
The research has been published in the journal Nature Communications, and it was led by scientists from three institutions in the Netherlands: Utrecht University, the Erasmus Medical Center, and the pharmaceutical company Harbour BioMed.
Since the emergence of the virus that causes COVID-19 — called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) — and the rapid spread of the disease throughout the world, scientists have been researching ways to fight back.
While much attention has focused on the creation of a vaccine that would enable the body to develop its own antibodies to the virus, researchers have also been working to develop the antibodies themselves, which could then be injected to help people combat the infection.
Previous research has shown that antibodies can help treat illnesses caused by similar viruses, so a SARS-CoV-2 antibody may help inhibit the infection until a vaccine is developed.
Generally, antibodies work by stopping a virus from infecting the cells of a host organism. According to the present study, the newly identified antibody stops SARS-CoV-2 from infecting cells by targeting the spike proteins on the virus’ surface that allow it to gain access to the cells of the host.
Antibodies are usually developed in nonhuman species. Researchers then take steps to make them effective within humans. However, the team has developed the new antibodies in a way that will not require “humanizing” them first.
While translating these findings into an effective COVID-19 treatment will require more research and testing, the initial discovery is valuable.
According to co-supervising study author Prof. Frank Grosveld, “This discovery provides a strong foundation for additional research to characterize this antibody and begin development as a potential COVID-19 treatment.”
“The antibody used in this work is ‘fully human,’ allowing development to proceed more rapidly and reducing the potential for immune-related side effects.”
Previously, the researchers had studied the outbreak of severe acute respiratory syndrome, or SARS, in 2002–2003. The coronavirus responsible for this disease has many similarities to SARS-CoV-2, so the scientists were able to build on their earlier research as they worked to identify a SARS-CoV-2 antibody.
Online Int’l News with additional input by GVS News Desk