Researchers at the University of Connecticut are looking into how an enzyme in the COVID-19 virus may be helping it mutate.
In recent weeks, variants of the coronavirus have emerged from the U.K., South Africa, and Brazil. These virus variants raise concerns about vaccine efficacy and increased transmission, among other things. Scientists are still researching how, exactly, these viruses came to mutate.
Sandra Weller is a professor and chair of the Department of Molecular Biology and Biophysics at UConn Health. While most of Weller’s past research has focused on the herpes simplex virus, Weller is now teaming up with researchers at Vanderbilt University Medical Center led by virologist Mark Denison.
The research is focused on recombination. Recombination occurs when an organism, such as the coronavirus, reproduces, and one part of its genome gets mixed with another part of its genome. This causes new features to emerge in the organism. Some scientists have suggested a critical reason the coronavirus was able to make a jump from animals to humans was because of recombination affecting the ‘spike’ of the virus, which is the part of the virus that allows it to enter human cells.
In a recent study, Denison and other researchers looked at recombination in other coronaviruses, and how it affects their spread. The study found an enzyme called nsp14-ExoN could be playing a part in recombination, and neutralizing the enzyme could reduce recombination. Weller and Denison are now working together to see if this could help in the treatment of COVID-19 patients.
Weller, Denison and others are now researching drugs that could help block nsp14-ExoN. This would in turn reduce recombination, which could stop the coronavirus from mutating and allow other drugs to work more effectively.
Weller told The New York Times nsp14-ExoN is shared across many coronaviruses. While this research is still in its early stages, this could mean protection from several viruses, not just COVID-19.
