protease inhibitors are a major part of what was being demonstrated here.
the spike protien docks with the human ACE2 enzyme, that is for certain. this is only one part of the entry process.
after docking the spike protien must be "cut loose" [primed] in order to allow the membrane fusion process to proceed. this cutting occurs at the behest of exocytic serine protease, named [TMPRSS2].
the function of TMPRSS2 is not very clear but it seems to facilitate viral entry of SARS-2, Thus serine protease interaction must be manipulated in addition to interfering with ACE2 docking.
Then there is the damage. ACE2 sweeps up angiotensins I, and II and converts them into a nonactive form thus regulating the angiotensin pool created by ACE.
when angiotensin II reaches its receptor [ATR] the immediate functional effect is to cause vasoconstriction and increase blood pressure to operational level.
when ACE2 is disrupted from managing the angiotensin II pool there is an excess of ATR activation and this leads to a pathological state. The space between lung epithelial cells becomes reinforced with extracellular fibres leading to pulmonary sclerosis in addition to widespread cell death in lung tissue.
this is where the concept of ACE inhibitor and ATR blockers come into play. the reduction of angiotensinII and reduction of ATR signalling is thought to be a method of mediating this pathophysiological consequence of initial ACE2 disruption during viral docking process.
the whole picture is to block the virus ability to dock, and block virus ability to initiate the fusion process; And to mediate damages caused by the disruption of the RAS by way of ACE inhibitors and ATR blocking.
that means four points of leverege in this system, require four drugs minimum and clinical care for patient management.