Why are Variants More Infectious?
November 10, 2021
New insights into the SARS-CoV-2 virus indicate that mutations in the alpha and delta variants may boost the virus’s ability to spread. Spike proteins are responsible for invading cells, but it’s been unclear how mutation alters the virus’s function. New research funded by the NIH focuses on the infectivity of both the alpha and delta variants, which will provide a framework for future treatment options as the virus continues to mutate.
SARS-CoV-2 contains a unique set of amino acids that is not present in other coronaviruses, with the spike protein present in the outermost layer and being responsible for binding to host cells. Before this can happen, “the spike protein must be activated by a series of cuts, or cleavages, by host proteins” (1). In both the alpha and delta variants, mutations appear to change a specific novel cleavage site, called the furin cleavage. These changes are thought to make the virus more effective at invading cells.
Researchers were able to show that this specific type of cleavage in the alpha and delta variants go “unchecked.” Researchers also observed the cells’ tendency to fuse with surrounding cells, “a behavior that may facilitate spread of the virus during infection.” Additionally, cells with mutated spike proteins fused with their neighbors more often than the original, “wild-type” spike protein. This indicates that mutations do enhance the virus’ ability to attach to and invade cells. While research was first conducted in fruit fly and mammalian cells, the team analyzed cells from healthy volunteers to find that the enzymes which impact cleavages could influence the severity of infection in humans. It was hypothesized that a person’s expression of these enzymes could also affect the virus’ ability to spread.