The hubbub around mutations in the virus that causes COVID-19—and how they might make it more infectious—has been around since the early phase of the pandemic. A preprint study about a particular mutation involving the “spikes” studding the SARS-CoV-2 pathogen had previously drawn attention, and that investigation has now been peer-reviewed and published in Cell. The paper details a change in one amino acid in the virus that may have made it more infectious. But virologists are far from a consensus about the possible role of this mutation.
The paper indicates that a single amino acid change from D (aspartic acid) to G (glycine) on the SARS-CoV-2 spike protein (which such viruses use to grab onto human cells) is the key to how infectious the pathogen is. “The spike protein has a critically important role in the biology of the virus,” says Bette Korber, a computational biologist at the Los Alamos National Laboratory and lead author of the new paper.
Korber and her colleagues came to this conclusion after employing multiple approaches to examine the two strains. First, they performed a statistical analysis that showed how the mutated virus—often referred to as the “G strain”—achieved dominance across multiple continents, outperforming the coexisting original version of SARS-CoV-2, or “D strain.” Then the researchers tested the amount of the virus in individuals with COVID-19 at the Sheffield Teaching Hospitals NHS Foundation Trust in England. The results showed that the G strain produced more of the virus in the human body than the D strain. But the former did not lead to a higher hospitalization rate, meaning it apparently did not cause more severe illnesses. Lastly, the team members created “pseudotype” pathogens by embedding SARS-CoV-2 spike proteins, containing either D or G amino acids, into other disease-causing viruses. They tested these pseudotype viruses by infecting human cells in a lab dish, and the result suggested that the G-bearing one was more infectious. Examining cells in a dish, however, is not the same as testing them using “multiple cell types with an immune system in a human body,” says Emma Hodcroft, a molecular epidemiologist at the University of Basel in Switzerland, who was not involved in the study. “We just have to be really careful with how far we take the conclusions.”
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