The anti-pancreatitis drugs Camostat and Nafamostat block SARS-CoV-2 replication in lung tissue (IMAGE)
Caption
(A) SARS-CoV-2 attaches to human cells through binding of its spike protein to the cellular protein ACE2. Next, SARS-CoV-2 exploits human enzymes like the protease TMPRSS2 for the activation of its spike protein, which subsequently fuses the viral membrane with a target cell membrane and thus allow the delivery of the viral genetic information into the cell. (B) Apart from TMPRSS2, SARS-CoV-2 can utilize other proteases for spike protein activation. Among them are TMPRSS11D and TMPRSS13, which are mainly expressed in the upper respiratory tract. The anti-pancreatitis drugs Camostat (as well as its metabolite GBPA) and Nafamostat not only block TMPRSS2 but also TMPRSS11D and TMPRSS13. As a consequence, switching from TMPRSS2 to TMPRSS11D or TMPRSS13 as activators does not allow SARS-CoV-2 to escape Camostat's/Nafamostat's antiviral activity.
Credit
Markus Hoffmann
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