You might not want to be taking EGCG now that coronavirus is afoot

Where are you seeing vitamin C is inhibiting EGCG's redox conversion? That study was saying that vitamin C inhibited EGCG's ACE inhibiting effects, not EGCG's entire redox cycle. I suppose it could be inhibiting it in some way, but I don't believe that is what the study I linked was claiming. Vitamin C could be counteracting the ACE effects by some other mechanism, while not affecting the zinc ionophore effects. Then you could still be getting the zinc transport benefits of the EGCG, but not any of the ACE inhibition.

Let's break it down a bit and see if we can figure out what is going on. So ACE2 is a zinc metalloenzyme and carboxypeptidase. I assume that it being a carboxypeptidase is how the SARS-CoV-2 virus is able to bind to the S1 receptor binding domain of the ACE2 enzyme using its spike protein (S-protein). The MERS-CoV virus did the same thing, but used the dipeptidyl peptidase 4 (DPP4) protein receptor instead of ACE2. These viruses have spike proteins that are expressed on the virus' membranes. This is what they use to grab a hold of ACE2 receptor proteins on the surface of respiratory cells. These are also the main target for your body's antibodies, which is why vaccines are targeting them. It looks like SARS-CoV-2 has two distinct spike proteins.

https://www.sciencedirect.com/science/article/pii/S0092867420302622

So what about zinc and ACE2? Well ACE2 contains a single zinc-binding domain HEXXH (His-Glu-X-X-His). So zinc itself is binding to ACE2. However, it does not appear that binding is inhibited by ACE inhibitors.

https://www.ahajournals.org/doi/full/10.1161/01.HYP.0000185149.56516.0a

https://sci-hub.tw/10.1007/s00109-003-0419-x

So ACE inhibitors are not blocking zinc itself from binding to its binding site on ACE2, which is good. One of the possible mechanisms for EGCG's ACE inhibition is chelation of zinc at the binding site of ACE. They are not certain on the exact mechanism yet, though. So what does this mean for COVID-19? Well let's look at chloroquine and how it it working. Well as we said, chloroquine is a zinc ionophore, or is helping to transport zinc to sites it is needed.

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109180

So that is exactly what EGCG is doing, too. It's chelating with zinc, and shuttling it to the places it needs to be. In the case of COVID-19, that's the ACE2 enzyme protein receptors in the surface of respiratory cells. It seems they are both working on similar mechanisms to essentially shuttle zinc into respiratory cells. Absorbic acid (vitamin C) can chelate zinc, too. It's actually pretty crucial to maintaining the redox cycle in cells. So the question then becomes if vitamin C is somehow preventing EGCG from chelating with zinc too, and shuttling it into the receptor binding domain of the ACE2 receptor. I suppose it is possible. However, I think the combo of zinc, EGCG, and vitamin C would be good to maintain that balance and prevent the immune system from going too far. I certainly don't think they are just cancelling each other out.

So it's definitely not settled yet. However, the mechanisms behind how SARS-CoV-2's spike protein is binding to the protein receptor site of the ACE2 enzyme, and how zinc and things like chloroquine play into that, make a lot more sense to me now. Perhaps chloroquine is simply chelating with zinc, shuttling it to the HEXXH binding site of the ACE2 enzyme, and either blocking SARS-CoV-2 from binding, or causing an immune response that brings antibodies to the site to fight it.