How to help the Alpha variant ‘dominate’ in the US

A new study shows that the strain first identified in the UK – B.1.1.7, new name Alpha – has the ability to ‘stealth’, hiding from the human immune system.
In December 2020, scientists first discovered a new strain of corona virus spreading in the UK. As this variant – known as B.1.1.7, with the new name Alpha – started to appear in many other countries, it became more difficult to control than when it first became known.

From April to now, Alpha has become the dominant strain in the US. Alpha’s superiority made scientists wonder why this virus strain spread so quickly. Recently, a study published online on June 7 was New York Times The quote has found the “secret of success” of this mutation: Alpha disables the first immune “stronghold” gland in the human body, giving the virus more time to multiply when it enters the body. up quickly. The Alpha mutation once made the UK crippled. Photo: Reuters. “Turn off the bell” alert Alpha has a total of 23 mutations – what sets it apart from other coronavirus strains. When this strain began to spread widely in the UK, researchers began examining the genetic sequence to look for an explanation of why it spread faster than other strains. Many researchers focused on nine mutations that change the proteins that coat the coronavirus and allow them to enter cells. One of those mutations helps the virus bind more closely to these cells, increasing the likelihood of successful infection. But other scientists focus on how Alpha affects the human immune response. Virologist Gregory Towers and colleagues at University College London cultured the coronavirus in human lung cells. They compared cells infected with Alpha with those infected with previous variants of the coronavirus. The team found that alpha-containing lung cells produced less interferon. Interferon is a protein produced naturally by cells in the immune system. They also found that in cells with Alpha, defense genes activated by interferon were less effective than in cells infected with other strains. Somehow, the most important “alarm bell” of the immune system barely “sounds” in the presence of the Alpha variant. “It becomes almost invisible (when it enters the human body),” Dr. Towers said. The UK has to impose strict restrictions because the strain B.1.1.7 spreads quickly. Photo: LBC. To find out how Alpha achieves this “invisibility,” the researchers looked at how the coronavirus replicates inside infected cells. They found that Alpha-infected cells made a lot of extra copies – about 80 times more than other variants – of a gene called Orf9b. According to previous research by molecular biologist Nevan Krogan and colleagues at the University of California, San Francisco, Orf9b makes a viral protein that attacks Tom70 — a protein needed to release interferon when the virus enters the body. body. From all of these studies, Dr. Krogan concluded that the Alpha variant contained a mutation that produced more Orf9b protein than normal. The Orf9b protein surrounds the Tom70 protein, reducing interferon production. The infected virus is no longer hindered by the immune system, so it rapidly multiplies in the human body. About 12 hours after infection, the immune system starts working again. Therefore, Dr. Towers speculates, people infected with Alpha have a stronger response than those infected with other strains. The virus-laden mucus lingers in both their oral and nasal cavities, making Alpha more contagious than ever. However, Dr. Laurent-Rolle insists more evidence is needed to support this conclusion. For example, scientists have not yet run a standard test to test the amount of the Orf9b protein. Dr. Krogan said he and his colleagues are looking to practice that experiment now. Totally different Dr. Krogan’s group also started similar tests on other strains, including the strain first identified in South Africa, called Beta (B.1.351) and the first identified strain. first in India, called Delta (B.1.617.2). The preliminary results surprised them. Both Beta and Delta reduce interferon in infected cells. But there is no indication that these two strains did so in the same way that Alpha did. Each strain evolved in a different way to control the immune system. Virus mutant particles B.1.1.7 from patient samples in the laboratory. Photo: NIAID. Cecile King, an immunologist at the Garvan Institute for Medical Research in Sydney, Australia, stressed that understanding how the virus evades the immune system will help in the development of a Covid-19 vaccine. Vaccines now help the immune system recognize mutated proteins. But research on patients recovering from Covid-19 shows that their immune systems learn to recognize viral proteins, including Orf9b. Some researchers are looking to include the coronavirus protein in a new vaccine. But this process needs care because some proteins reduce immunity. “It’s a pretty complicated process. But if we take a closer look, it might be possible,” Dr. King said.