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Experimental Drug Blocks COVID-19 Viral Entry Into Lung Cells
An experimental compound prevents the virus that causes coronavirus disease 2019 (COVID-19) from entering human airway cells, a new study finds.
An experimental compound prevents the virus that causes coronavirus disease 2019 (COVID-19) from entering human airway cells, a new study finds.
Posted online recently on the preprint server bioRxiv, the work revolves around the structure of SARS-CoV-2, the virus causing the current pandemic. This virus has on its surface a spike protein that can attach to angiotensin converting enzyme 2 (ACE2), a protein on the surface of cells lining human lungs. Once attached, the spike pulls the virus close to a cell, which lets it fuse to it and enter it, and then hijack the cell’s machinery to make copies of itself, researchers say.
For this reason, molecular biologists have sought to engineer forms of ACE2 that, instead of being woven onto the cell surface, float freely. They hoped that free-floating ACE2 could serve as a decoy that competes with the membrane-bound counterpart for the viral spike protein, thereby blocking virus entry.
Led by researchers at NYU Grossman School of Medicine, a new investigative effort made key changes to a free ACE2 molecule, and then fused one part of it to a piece of an antibody, an immune system protein, with the goal of strengthening its antiviral effect. The team calls their molecule an “ACE-2 microbody.”
