Yeah, normally I don't put too much weight on molecular simulations since the actual in vivo mechanisms can be thoroughly complex, but this makes a lot of sense.
Another hypothesis is the Bradykinin inhibition from ACE 2 being removed because the virus uses ACE 2 receptors to enter the cell. So no ACE 2 means lots of Bradykinin, which makes blood vessels leaky.
So not only is there inflammation but you are literally drowning in your own juicy liquids leaking from the inflamed blood vessels.
I'm think there is something to ACE2 Bradykinin inhibition disruption. My possible COVID experience involved sudden vasodilation and BP drops. Was really weird.
Yeah, normally I don't put too much weight on molecular simulations since the actual in vivo mechanisms can be thoroughly complex, but this makes a lot of sense.
Another hypothesis is the Bradykinin inhibition from ACE 2 being removed because the virus uses ACE 2 receptors to enter the cell. So no ACE 2 means lots of Bradykinin, which makes blood vessels leaky.
So not only is there inflammation but you are literally drowning in your own juicy liquids leaking from the inflamed blood vessels.
What a wonderful engineered virus this is.
I'm think there is something to ACE2 Bradykinin inhibition disruption. My possible COVID experience involved sudden vasodilation and BP drops. Was really weird.