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How the ‘alpha’ coronavirus is so powerful

in december British researchers discovered that a new variant was spreading across the country. When it comes to other countries, this variant, now known as Alpha, is likely to become commonplace in new homes as well. in April It has become the main variable in the United States. and since then

Alpha’s rapid success has led scientists to wonder how such variables conquered the world. A new study sheds light on one secret of its success: Alpha shuts down our body’s first line of immune defense. This gives the variable more time to multiply.

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Dr. Maudry Laurent-Rolle “It’s very impressive,” said a doctor and virus specialist at the Yale School of Medicine who wasn̵

7;t involved in the new study. must be superior to that first defense system The more successful it is in doing so, the better the virus is.”

The report was posted online Monday and has not yet been published in a scientific journal.

Alpha has 23 mutations that differentiate it from other coronaviruses. When the variables start to increase in the UK Researchers are beginning to examine these genetic modifications to find an explanation for why they spread faster than other variants.

Many researchers have focused on nine mutations that alter a protein called spike that covers the coronavirus and allows it to invade cells. One of these mutations helps the virus bind to cells more tightly. This may increase your chances of being infected successfully.

But other scientists have highlighted how alpha affects the human immune response. Gregory Towers, a virus specialist at University College London, and his colleagues created coronavirus in human lung cells By comparing Alpha-infected cells with earlier coronavirus-infected cells.

They found that alpha-lung cells produced significantly less interferon. which is a protein that stimulates a large amount of immunity They also found that in alpha cells The protective genes normally switched on by interferon were quieter in cells infected with other variants.

However, the immune system’s most important alarm bell rarely sounds when there is an alpha variant. “It makes itself more invisible,” Towers said.

to examine how Alpha achieves this invisibility. Researchers have looked at how the coronavirus replicates inside infected cells. They found that alpha-infected cells produced many extra copies. That’s about 80 times more than other versions of the virus from a gene called Orf9b.

Nevan Krogan, a molecular biologist at the University of California, San Francisco and co-author of the new study, said: “It’s not on the chart.

In previous research, Krogan and his colleagues found that Orf9b builds a viral protein that locks into a human protein called Tom70, and it so happens that Tom70 is needed for the cell’s interferon release when faced. with invading viruses

Taking all the evidence together, Krogan and his colleagues argued that the alpha variant had mutations that forced the production of more Orf9b proteins. Those proteins clustered on the human Tom70 protein, reducing interferon production. and full immune response Viruses that are protected from attacks have a better chance of creating copies of themselves.

However, the infected cells were able to gradually eliminate the Orf9b protein from its Tom70 molecule about 12 hours after infection. The alarm system will start to come back online again. And because of that immune response, Towers said, “All hell is freed.”

Towers predicted when a delayed immune response eventually occurred. Alpha-infected people react more severely than with other variants. Not only that, coughing and expelling viral-infected phlegm from their mouths. but also the nose Make Alpha work better spread.

“What they showed made sense,” Laurent-Rolle said, but she wanted to see more evidence to support their conclusions. For example, scientists did not perform standard tests to measure the amount of Orf9b protein.

“That’s one concern,” she said. Krogan said he and his colleagues are currently developing that test.

Krogan’s team also began similar experiments in other variants, including the first identified variant in South Africa, known as beta, and another identified in India, known as Delta. The initial results surprised them.

Both beta and delta drive interferons in infected cells. But there is no sign of doing so by filling cells with the Orf9b protein. They may have developed their own tricks to manipulate our immune system independently.

“They’re attenuating the immune response in different ways,” Krogan said.

Cecile King, an immunologist at the Garvan Institute of Medical Research in Sydney, Australia. Who was not involved in the study said understanding how the virus develops these escape methods. It will help scientists design better vaccines for COVID-19.

Current vaccines instruct the immune system to recognize the ejected protein. But studies on people recovering naturally from COVID-19 show that their immune systems learn to recognize other viral proteins, including Orf9b.

A number of researchers are integrating coronavirus proteins into a new vaccine. But they need to be careful because certain proteins can weaken immunity.

“It’s a tricky business. But it becomes more possible as we learn more,” King said.

This article originally appeared in The New York Times.

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