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A protein that raises death risk can be used to stop infection and “cure” illness – scientists

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The findings not only answer key questions why elderly and patients with preexisting medical conditions including diabetes, hypertension, obesity, metabolic syndrome, cardiovascular disease and chronic lung diseases like COPD and asthma are at higher death risk, but also outline implications for the development of therapeutics to control viral infection.

Brown University researchers outline the physiological and molecular events that explain why these populations have a higher risk of infection, severe side effects, and death in a new study published in the journal JCI Insight.

The findings show that a protein called chitinase 3-like-1 increase with age as well as co-morbid diseases and infection not only help to understand key mechanisms of the complex SARS-CoV-2 virus, as explained by the study author, but also have direct implications for the development of therapeutics to control the viral infection.

Scientists from the National Institutes of Health-funded Elias laboratory, including lead study author Suchitra Kamle and co-author Chun Geun Lee, have recently concentrated on the biology of chitinases and chitinase-like proteins, which are enzymes and enzyme-like molecules, respectively. A chitinase-like protein called chitinase 3-like-1, which is naturally found in blood, is of particular interest.

Chitinase 3-like-1 is a key component of a pathway that is activated in response to injury and inflammation. These and other researchers have discovered that circulation levels of chitinase 3-like-1 rise after infection, particularly in disorders defined by inflammation and tissue changes, such as emphysema, asthma, and COPD, which are all risk factors for COVID-19.

Interestingly, levels of chitinase 3-like-1 have been reported to rise with natural ageing, according to Lee. Among fact, they’ve been found to be the most accurate predictor of all-cause mortality in adults in their eighties.

According to Elias, the researchers thought they might be able to apply some of the work they’ve already done with this gene family to COVID-19. They chose to look into the connection between chitinase 3-like-1 and the ACE2 receptor, which the SARS-CoV-2 attaches to in order to enter human cells.

The researchers compared the effects of chitinase 3-like-1 on ACE2 and other protease enzymes that metabolise the spike protein and contribute to infection in a series of trials. They looked at these interactions in the lungs of mice with increased amounts of chitinase 3-like-1 as well as mice that were lacking in chitinase 3-like-1. Kamle oversaw experiments in the lab that looked at the impact of chitinase 3-like-1 on human lung epithelial cells.

Chitinase 3-like-1 levels rose with age, co-morbid conditions, and infection, according to the study. Furthermore, they discovered that chitinase 3-like-1 was a powerful activator of the SARS-CoV-2 receptor, which is used to infect cells.

Following this discovery, the researchers created FRG, a humanised monoclonal antibody that targets a specific area of chitinase 3-like-1, which proved out to be crucial. They discovered that this “therapeutic” antibody, as well as another small chemical, effectively prevented ACE2 receptor induction.

“So in that way, the virus cannot enter into the host system,” said Kamle, adding, “this means there will be less infection in the presence of this therapeutic FRG antibody.”

“You can imagine a scenario in which someone who has been exposed to a person who has the virus is given the antibody, which then acts like a prophylactic to prevent infection or make the symptoms that the infection induces milder,” he said.

Another possible scenario, according to the authors, is that the virus-infected person is given the antibody or tiny chemical, which effectively “cure” the condition by stopping the infection.

“We show in this paper that if we make antibodies or other small molecules that can inhibit chitinase 3-like-1, they can be therapeutics to control viral infection,” they said.

Image Credit: Getty

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