To enter and infect human cells, surface proteins on the SARS-CoV-2 virus must be modified by an enzyme called TMPRSS2 in the lung. This protein can be effectively targeted by an existing drug that may therefore constitute a treatment option.
Hoffmann M. et al., SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell (2020). doi: 10.1016/j.cell.2020.02.052. [Epub ahead of print]
In press April 16, 2020
For viral entry to occur, spike proteins on the surface of a SARS-CoV-2 particle must attach to its receptor, angiotensin-converting enzyme 2, on the surface of a host cell. This binding is dependent on appropriate processing of the spike by the host enzyme TMPRSS2. The clinically-proven drug camostat mesylate was previously reported to be effective in inhibiting TMPRSS2. Here, the authors found that camostat was extremely effective in inhibiting entry of SARS-CoV-2 into fibroblast cells. Additionally, the authors report that antibodies raised against the spike protein of SARS-CoV (which emerged in 2002) can cross neutralize SARS-CoV-2 particles, meaning that they can stop spike proteins from attaching to host cells. Antibodies against SARS-CoV may therefore offer some protection against SARS-CoV-2 virus too.
Summary by Sivakami Mylvaganam