UCSD researchers discovered carbohydrates in the lungs that use COVID-19

Photo by Zoë Meyers / inewsource

Above: The UC San Diego School of Medicine campus is shown on February 1, 2020.

Researchers at UC San Diego School of Medicine announced on Tuesday that they had discovered a carbohydrate that the SARS-CoV-2 virus uses to latch onto a cellular molecule in the lung, treating COVID-19 patients. Has potential effects.

Since January, researchers have discovered that the novel coronovirus primarily uses a molecule called ACE2 – which sits on the outer surfaces of cells like a dorknob that lines the lungs – to enter and infect those cells for. Finding a way to close the interaction between the virus and dorknob as a means of treating the infection has become the goal of many research studies.

UCSD researchers recently discovered that the virus cannot capture the ACE2 dorknob without the carbohydrate heparan sulfate, which is also found on lung cell surfaces.

“ACE2 is only part of the story,” said Jeffrey Esko, a professor of cellular and molecular medicine at UCSD and co-director of the Center for Glycology Research and Training. “It’s not the whole picture.”

Esko’s study, published in the academic journal Cell, introduces a potential new approach to preventing and treating COVID-19.

His team demonstrated two approaches that could reduce the capacity of viruses to human cells cultured in the lab by about 80 to 90%, either removing heparan sulfate with enzymes or using heparin as bait. Can and bind coronavirus to human cells.

Heparin, a form of heparan sulfate, is an already widely used drug to prevent and treat blood clots.

Esco’s team has studied heparan sulfate for a long time and the role it plays in health and disease.

The team found that the virus binds heparin. When heparin is bound, the virus is able to bind ACE2. Researchers found that the virus, heparan sulfate, should bind on both the cell surface and ACE2, so that it could be found inside laboratory-generated human lung cells.

With the establishment of this viral entry mechanism, researchers set next about trying to disrupt it. They found that enzymes that remove heparan sulfate from the cell surface prevent SARS-CoV-2 from entering cells. Similarly, treatment with heparin also prevented infection. Heparin treatment acted as an anti-viral in the doses currently being given to patients, even when researchers removed the anticoagulant region of the protein – the part responsible for preventing blood clots.

Esco warns that the findings are still far from translating into a COVID-19 treatment for people.

Researchers will need to test heparin and heparan sulfate inhibitors in animal models of SARS-CoV-2 infection. In a related study, UC San Diego scientists are also exploring the role of the human microbiome, which includes bacteria that live on the body, play a role in changing heparan sulfate and thus a person’s susceptibility to COVID-19 Affect.

“This is one of the most exciting times of my career – everything we’ve learned about heparan sulfate and the resources we’ve developed over the years have come together with a wide variety of experts from many institutions, who collaborate. Look forward to doing. And share ideas, “said Esko.

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