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Researchers discovered the Alpha variant used a specific protein to avoid an immune response

New research investigating how the first variant of interest of the new coronavirus evolved has found that the Alpha variant evolved mutations that suppress specific aspects of the immune system, similar to mutations in the immune system. variable seen in newer variants such as Omicron.

The Alpha variant first appeared in the UK in autumn 2020, introducing the world to the dreaded idea of ​​variants of SARS-CoV-2, the virus that causes COVID-19. Although it has since been far behind by subsequent variants including Delta and Omicron, studying Alpha’s structure and function helps scientists better understand how virus variants evolve. .

Researchers from the US and UK worked together to investigate how Alpha attacks the human body, and discovered that the mutations that allow it to evolve go far beyond those centered around the mutant protein. Out.

Their study, described in the journal Nature on Thursday, found that the Alpha variant boosts the production of a specific protein that can help it block the way infected cells signal the immune system. immune system.

To dig deeper into how the Alpha variant works, the researchers looked at lab-grown cells infected with the variant to monitor protein levels and how the cells function. .

They then compared the data with how the cells responded to infection with the original COVID-19 strain. The biggest difference is in the way the body’s innate immune response – or not. This is the body’s first line of defense, to prevent pathogens from entering. Alpha interfered with the rallying cry that normally activates this system, the researchers say.

Inside Alpha-infected cells are a multitude of three viral proteins known to help COVID-19 evade an immune response. One in particular, called Orf9b, achieves this by blocking a protein in our cells that normally turns on genes that signal our immune system to respond.

In the study, the researchers say this type of mutation may contribute to the enhanced transmissibility of the Alpha variant by suppressing more of the initial immune response, which could allow the variant to reactivate. create faster.

These findings suggest that the mutated protein is not the only factor that researchers should think about when designing treatments to help people infected with COVID-19.

Because SARS-CoV-2 uses mutant proteins on its surface to attach to receptors in a person’s cells, mutations around mutant proteins are more commonly talked about than others. With the Delta variant, a more efficient mutant protein is thought to help it better bind to our cells, and all current COVID-19 vaccines are targeted to these cells. our own immune response against this mutant protein.

Devan Krogan, one of the paper’s authors and head of the University of California San Francisco’s Institute of Quantitative Biological Sciences (QBI) and the Coronavirus Research Group (QCRG), said in a statement. newspapers.

“But what happens after the virus enters the cell? There may be other mutations that allow it to reproduce more.”

Although each variant is different, many share similar mutations, with both Delta and Omicron appearing as cousins ​​of the Alpha variant. Delta and Omicron both have similar mutations in the areas where the researchers studied the Alpha variant, which means they may have similar effects on the immune system.

“The virus will continue to evolve and adapt to the host, and each time it will adapt better and better,” said Lorena Zuliani-Alvarez, co-author and senior scientist at QBI. “That’s why Omicron has 53 mutations.”

The study shows that studying mutations outside of those around the mutant protein will give scientists a more complete picture of the virus as it evolves, something that will be crucial in combating the virus. future variations.

Mehdi Bouhaddou, a postdoctoral scholar and co-author, said: “Studying the variants that are of interest to us will give us an idea of ​​how SARS-CoV-2 evolves. “We now know about the proteins that mutate most frequently and the biological consequences of those mutations. I think this helps us prepare for what could happen next.”

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