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How the “alpha” version of the coronavirus became so powerful

In December, British researchers discovered that a new option covered their country. When it arrived in other countries, the variant, now known as Alpha, tended to be more common in its new homes. By April, it had become the dominant option in the United States and has remained so ever since.

Alpha’s rapid success has left scientists wondering how the option has taken over the world. A new study reveals a secret to its success: Alpha deactivates the first line of immune defense in our bodies, giving the variant more time to reproduce.

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“It’s very impressive,” said Dr. Modri ​​Laurent-Roll, a doctor and virus expert at Yale Medical School who was not involved in the new study. “Every successful virus must go beyond this first defense system. The more successful it is, the better the virus. “

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

Alpha has 23 mutations that distinguish it from other coronaviruses. When the variant began to grow in the UK, researchers began checking for these genetic changes to look for explanations as to why it was spreading faster than other variants.

Many researchers have focused on the nine mutations that alter the so-called spike protein that covers the coronavirus and allows it to invade cells. One of these mutations helps the virus bind more closely to cells, potentially improving its chances of successful infection.

But other scientists have focused on how Alpha affects the human immune response. Gregory Towers, a virus expert at University College London, and his colleagues grow coronaviruses in human lung cells, comparing Alpha-infected cells with those infected with earlier versions of the coronavirus.

They found that alpha lung cells produced drastically less interferon, a protein that includes multiple immune defenses. They also found that in alpha cells, the protective genes that are normally turned on by interferon are quieter than in cells infected with other variants.

Somehow the most important alarm bells barely rang in the presence of the alpha variant. “It̵

7;s becoming more invisible,” Towers said.

To study how Alpha achieved this invisibility, the researchers looked at how the coronavirus replicated in infected cells. They found that alpha-infected cells made many additional copies – about 80 times more than other versions of the virus – of a gene called Orf9b.

“It’s off the chart,” said Nevan Krogan, a molecular biologist at the University of California, San Francisco and co-author of the new study.

In previous studies, Krogan and colleagues found that Orf9b produced a viral protein that locked to a human protein called Tom70. And that’s exactly what happens, Tom70 is essential for the release of interferon from the cell in the face of an invading virus.

Gathering all the evidence, Krogan and colleagues claim that the alpha variant carries a mutation that forces the production of many more Orf9b proteins. These proteins swarm human Tom70 proteins, reducing interferon production and the overall immune response. An attack-protected virus has a better chance of making copies of itself.

However, the infected cell can gradually remove the Orf9b proteins from its Tom70 molecules. Approximately 12 hours after infection, the alarm system begins to return online. And because of that immune response, Towers said, “all hell is falling apart.”

Towers speculates that when the delayed immune response finally occurs, people infected with alpha have a stronger reaction than other variants, coughing and secreting virus-laden mucus not only from their mouths but also from their noses. alpha even better spread.

“What they’re showing makes sense,” Laurent-Roll said. But she would like to see more lines of evidence to support their conclusion. For example, the researchers did not perform a standard test to measure the number of Orf9b proteins.

“It’s one thing that could be related to that,” she said. Krogan said he and his colleagues are developing this test now.

Krogan’s team has also begun similar experiments with other variants, including the variant first identified in South Africa, known as Beta, and the one first identified in India, known as Delta. Preliminary results surprised them.

Both Beta and Delta release interferon into infected cells. But there is no indication that they are doing this by flooding the cells with Orf9b proteins. They may have developed their own tricks to manipulate our immune system.

“They all refuse the immune response in different ways,” Krogan said.

Cecil King, an immunologist at the Raven Institute for Medical Research in Sydney, Australia, who was not involved in the study, said understanding how the virus evolved in these escapes would help scientists develop better vaccines for COVID-19.

The current harvest of vaccines directs the immune system to recognize thorn proteins. But studies on people recovering naturally from COVID-19 show that their immune systems are learning to recognize other viral proteins, including Orf9b.

A number of researchers have combined combinations of coronavirus proteins into new vaccines. But they need to be careful because some of the proteins can actually damage the immune system.

“It’s a pretty complex venture, but it becomes more possible when we learn more,” King said.

This article originally appeared in The New York Times.

© 2021 The New York Times Company

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