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BoughtByBloomberg 2 points ago +2 / -0

You're welcome. This is just a hypothesis at this point based on protein structures and the fact that chloroquine works by tricking a malaria parasite into eating it instead of eating hemoglobin, thus killing it.

So if Chloroquine works against Wu flu, then it would make sense that it would bind to viral particles, and if it can bind to particles then the viral particles can bind to heme, which in computer models, seems to be what it does!

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Scroon 1 point ago +2 / -1

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.

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BoughtByBloomberg 1 point ago +1 / -0

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.

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Scroon 1 point ago +2 / -1

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.