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The study, published in the journal Cell, used single-cell RNA sequencing, which identifies which of the approximately 20,000 genes are “turned on” in individual cells, and found that only a small percentage of human respiratory and intestinal cells produce the proteins that help The virus gains entry into human cells.
“We began to look at tissue cells, such as the lining of the nasal cavity, lungs, and intestine, based on reported symptoms and where the virus was detected,” said José Ordovas-Montanes, co-author of the Boston Children’s study . Hospital in the United States.
“We wanted to provide the best possible information across our spectrum of research models,” said Ordovas-Montanes.
Recent studies have pointed out that the new coronavirus, SARS-CoV-2, like the closely related SARS-CoV behind the SARS 2002-03 pandemic, uses a receptor called ACE2 to enter human cells, aided by an enzyme called TMPRSS2. .
In current research, scientists discovered that only a small fraction of cells, often well below 10 percent, produces both ACE2 and TMPRSS2.
They said these cells fall into three categories: goblet cells in the nose that secrete mucus, lung cells known as type II pneumocytes that help keep the sacs of alveoli where oxygen is taken, and a type of so-called enterocytes that line the little ones. intestine and helps in the absorption of nutrients.
“Many existing respiratory cell lines may not contain the full mix of cell types and may miss the types that are relevant,” said Ordovas-Montanes.
“Once you understand which cells are infected, you can begin to ask yourself, ‘How do these cells work?’ “Is there something inside these cells that is critical to the life cycle of the virus,” he explained.
With more studies, the researchers said they can make better screens to find which existing drugs attack COVID-19’s biological mechanism.
Ordovas-Montanes and his team also discovered that interferon, one of the body’s main defenses when it detects a virus, stimulates the ACE2 gene, which encodes the receptor used by SARS-CoV-2 to enter human cells.
They said that this signaling molecule used by cells to communicate with each other about the infection, activated the ACE2 gene at higher levels, potentially giving the virus new portals to enter.
“ACE2 is also essential to protect people during various types of lung injury,” said Ordovas-Montanes.
“When ACE2 appears, it is usually a productive response. But since the virus uses ACE2 as a target, we speculate that it could be exploiting that normal protective response,” he added.
And since interferon also plays a role in the body’s natural immune response against viruses, scientists believe that the time the molecule is active in the body compared to the virus infection process is key to its effects. .
“It could be that in some patients, due to timing or dose, interferon may contain the virus, while in others, interferon promotes more infection,” said Ordovas-Montanes.
“We want to better understand where the balance is and how we can maintain a productive antiviral response without producing more target cells for the virus to infect,” he added.
Scientists also believe it is too early to link the findings to the uncontrolled inflammatory response, called a cytokine storm, reported in very sick patients with COVID-19.
They explained that cytokines are a family of chemicals that stimulate the body’s immune responses to fight infection, adding that interferon is part of this family.
“It may be that we are seeing a cytokine storm due to a failure of interferon to restrict the virus, so the lungs begin to ask for more help. That is exactly what we are trying to understand at the moment,” Ordovas- Montanes said. .
This story has been published from a cable agency source without modification to the text. Only the owner has been changed.
