Why a variant of the coronavirus could signal a new global alert

A variant of the coronavirus rapid spread blunts the body’s first line of defense, which could explain why it is more transmissible than previously circulating variants, according to a study on the infection of cells with SARS-CoV-2.

Since it was first detected in the UK at the end of last year, the variant B.1.1.7, also called Alfa, has traveled the world to become the dominant form of SARS-CoV-2. Some studies show that Alpha’s ability to overcome previously circulating variants could come from mutations in its spike protein that allow it to enter cells more efficiently.

But a study published in bioRxiv June 7 suggests that the variant also has tricks related to mutations outside of the spike protein. These mutations probably mean that Within hours of infecting a person, Alpha suppresses the body’s rapid response defense against all invaders. By blocking this “innate immune response”, the virus buys itself more opportunities to infect other people, warns research published in the scientific journal Nature. This helps Alpha to “Treat or hide from innate immunity, and we think that’s important for transmission”, of Claire Jolly, virologist University College London, who co-directed the work.

Cheerful and his colleagues examined how cells in the human respiratory tract produce interferon, an immune protein that activates the body’s defenses against the arrival of a pathogen. The team found that cells infected with Alpha produce much less interferon than cells infected with previously circulating SARS-CoV-2 variants. Alpha suppression of interferon production helps the variant stay longer in the body.

Nosy protein

Alpha infected cells they also had much higher levels of viral RNA encoding the Orf9b protein and Orf9b itself. The researchers found that Orf9b dampens the body’s defenses by interfering with the host’s proteins which normally activate the production of interferon and other genes important for the innate immune response.

The conclusions of this research have not yet been peer reviewed, But another study published in bioRxiv on March 4 by Silvana Gaudiera, immunogeneticist University of Western Australia at Perth, and his colleagues corroborate some of these conclusions. Gaudiera and your team analyzed viral samples from people infected with Alpha and found significantly higher levels of RNA expression, probably representing the production of Orf9b, than in people infected with previous variants.

The team attributes this overexpression to a mutation outside the peak protein, in genes important for viral replication. The last article “Highlights the importance of looking beyond the protein peak in search of new mutations ”, of Gaudiera. These results have not been peer reviewed either.

Nevan Krogan, geneticist at the University of California at San Francisco, who co-directed the work with Cheerful, he says that researchers are now extending their analysis to other variants of interest. “This virus is super sneaky,” he says. “The question is, what other tips does he have?

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