The alpha variant SARS-CoV-2 – the first troubling variant of the coronavirus – has developed mutations that allow it to more effectively suppress the early immune response to infection, according to a new study led by scientists at the Institute for Quantitative Bioscience by UC San Francisco. (KBI) is the University of San Francisco. Born in London.
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The researchers found that this variant increased the production of a protein that is used to suppress immunostimulatory signals from infected cells.
The mutations responsible for this change probably help the Alpha variant to avoid immunological detection and accelerate its transmission, and importantly, similar mutations exist in Omicron. The results were published in the journal Nature and published Technology.
The team of scientists found that the increased infectivity of the alpha was caused by mutations outside the “stem”, proteins that have attracted most of the stumps of scientists since the beginning of the pandemic. .
Spike, which the virus uses to enter its host cells, is key to the infection and is the target of all available vaccines against kovid 19. But it is just one of many tools the virus uses to manipulate its host.
While scientists are closely monitoring mutations in the region of new variants – omicron has more than 30.
“Mutations in the cells allow the virus to enter the cells more effectively. But what happens after the virus enters the cells? Maybe there are other mutations that allow it to replicate more,” said a scientist, who also directs. the UCSF KBI and its coronavirus research. group (KCRG).
After it was first discovered in the UK in late 2020, Alpha spread rapidly around the world, suggesting that it was significantly more transmissible than the original virus.
Laboratory experiments have shown that the new variant does not replicate faster than its predecessor. Looking for an explanation, KCRG began to know if the new variant reacted differently with the infected cells.
The team, which also included researchers from the Massachusetts Institute of Technology (MIT), the European Molecular Biology Laboratory (EMBL) and the Icahn School of Medicine in Mount Sinai, compared the effect of the variant on to host cells with the virus isolated in the world. the early stages of the pandemic. .
To do this, postdoctoral scientists measure the activity of each gene and monitor protection levels in virus-infected cells cultured in the laboratory. They also examined the phosphorylation status of the protein – an analysis that revealed chemical modifications that could temporarily impair protein function.
Using these data to compare the response to infection with the original alpha and virus, the researchers found that many significant differences included an innate immune response, the body’s first line of defense against pathogens.
Many of the genes involved in the assembly of this defense have been readily activated in the presence of the SARS-CoV-2 alpha variant.
In addition, the team found that alpha-infected cells contain a large amount of three viral proteins that are known to help the virus prevent the body’s immune response.
Further experiments have shown that one of them, called Orf9b, performs this task by binding to a protein that includes genes that stimulate immunity.
He suggests that it is possible to help the immune system fight SARS-CoV-2 by developing drugs that block this interaction and offer a potential strategy for doing so.