Recombinant form of ACE2 reduced SARS-CoV-2 infection in cultured cells.
SARS-CoV-2 exploits a receptor on angiotensin-converting enzyme 2, or ACE2, to gain entry into cells. The virus binds to a cell’s ACE2 receptor and injects its genetic material into the cytosol so the virus can replicate. A recent study suggests that an experimental antiviral drug called APN01 might inhibit SARS-CoV-2’s capacity to bind with ACE2.
APN01, also known as human recombinant soluble angiotensin-converting enzyme 2, or hrsACE2, is a genetically engineered drug. A previous clinical trial demonstrated hrsACE2’s efficacy against acute respiratory distress syndrome, a common complication of SARS-CoV-2 infection.
The authors of the current study isolated SARS-CoV-2 from nasopharyngeal (roof of the mouth) samples taken from a patient in Sweden who tested positive for COVID-19. Then they infected cultured cells with the isolated virus with or without the presence of hrsACE2. Fifteen hours after infection, they found that hrsACE2 inhibited viral entry by a factor of 1,000-5,000 by impairing SARS-CoV-2’s ability to bind to the ACE2 receptor.
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These findings demonstrate that hrsACE2 shows promise as a therapeutic against COVID-19. Future clinical trials will further elucidate the drug’s efficacy in humans.