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Ohio State University investigators have found a way to trick 2019 coronavirus disease (COVID-19) into binding to a bogus ACE2 receptor so it cannot infect cells . The results were published in the journal Chemistry of bioconjugates.
“Our goal is that every time SARS-CoV-2 comes in contact with the peptides, the virus is inactivated. This is because the virus’s Spike protein is already bound to something it needs to bind to the cell, “Amit Sharma, co-lead author of the study and assistant professor of veterinary biosciences at the State of the Ohio. “In order to do that, we have to attack the virus while it is still outside the cell.”
Because the SARS-CoV-2 virus uses ACE2, a receptor protein on the surface of a target cell found in the lungs and nasal cavity, as an access point for infection, investigators wondered whether they would be able to develop a replica in which the virus binds to instead of the real one. COVID-19 binds extremely tightly to ACE2, which is one of the reasons the disease is so contagious.
To do this, the team looked at images of the SARS-CoV-2 spike protein and the ACE2 receptor, looking specifically at how they interact with each other and what is needed for them to lock into place. square. They found a small, ribbon-shaped tail that seemed to be the focal point of the attachment.
They then tested different fragments of proteins, called peptides, to see which had a secure binding to the COVID-19 spike protein, as well as an ability to prevent or reduce viral replication inside cell cultures. They found that 2 of the peptides, one with a large point of contact and one with a minimum of points, were able to do this.
“Most of the peptides we have designed are based on the ribbon in contact with the Spike,” Sharma said. “We focused on creating the shortest possible peptides with the minimum of essential contact.”
These findings are the start of a product development process that will be continued by other virologists and pharmaceutical chemists to try to develop them and find ways of implementing them in the fight against the disease.
“We take a multi-pronged approach,” said Sharma. “With these peptides, we have identified the minimum contacts necessary to inactivate the virus. In the future, we plan to focus on developing aspects of this technology for therapeutic purposes.”
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