Multiple studies are revealing why the SARS-CoV-2 variant is so transmissible, but also seems to cause milder disease.
Researchers have determined that despite its myriad mutations, Omicron’s spike protein binds tightly to the ACE2 receptor on a person’s cells.first detected in South Africa
last November, Omicron spread around the globe faster than any previous variant of the coronavirus SARS-CoV-2, readily infecting even those who had been vaccinated or previously had COVID-19. To learn how it was able to do this, scientists have turned to techniques such as cryo-electron microscopy, to visualize Omicron’s molecular structure at near-atomic resolution.
By comparing Omicron’s structure with that of the original version of SARS-CoV-2 and its other variants, they have begun to shed lighton which features of the highly mutated virus have enabled it to evade the body’s immune defences, while also maintaining its ability to attack a person’s cells. And they’ve begun to unpick why Omicron seems to cause milder disease than previous variants.
“Omicron is very different structurally than all the other variants we have known so far,” says Priyamvada Acharya, a structural biologist at the Duke Human Vaccine Institute in Durham, North Carolina.Omicron has dozens of mutations not seen in the original SARS-CoV-2 strain that researchers first detected in Wuhan, China. More than 30 of those mutations are in the spike protein on the coronavirus’s surface, which helps the virus to latch on to and infect host cells.
With such a big shift in shape, there’s a huge question over how Omicron can still bind strongly to ACE2. “Normally, when you have so many mutations all over, you expect that you will also have compromised the ability to bind the receptor,” says Sriram Subramaniam, a structural biologist at the University of British Columbia in Vancouver, Canada.
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