(Reuters) – When the SARS-CoV-2 spike breaks into cells via the ACE2 receptor, a second cell-surface protein called vimentin facilitates the process, possibly by serving as a bridge between the virus and ACE2, new research suggests.

Using sophisticated analytical chemistry techniques, the researchers observed that vimentin attaches itself to the spike protein on the surface of the coronavirus. Based on their findings, they believe it might also attach itself to the ACE2 protein. In test tube experiments, they saw that when both vimentin and ACE2 are present, entry of the virus into the cells that line the blood vessels increases. They also found that depletion of vimentin significantly reduces SARS-CoV-2 infection of human cells, according to a report published in PNAS.

Study coauthor Nader Rahimi of Boston University School of Medicine said his team found that a monoclonal antibody developed by Abcam Plc blocked vimentin from binding to the virus, in turn keeping the virus from entering the cells.

Vimentin is also found on cells lining the heart, the air sacs of the lungs, and the nose, the researchers noted.

“Establishing the full range of the involvement of vimentin in viral entry and infection will require further investigations,” the researchers said in a statement. They said they hope their findings will lead to new antiviral drugs that keep both ACE2 and vimentin from interacting with the coronavirus.

SOURCE: https://bit.ly/3HjIOyS PNAS, online January 25, 2022.

Source: Read Full Article