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While we have tussled, I think you are spot on with some of your commentary and some of your statements.

As for HCQ simply not working, as I said, I think it is a weak prophylactic. Utilizing it in early infection did not reduce progression to severe disease, nor hospital time. While this was early in the pandemic, it seems to have held. Early in the pandemic, we were looking for anything that would help anticipating that we would either find the so called silver bullet or something would be therapeutically developed. I will work on literature searches to find the data, but most health care systems abandoned HCQ for therapy for hospitalized patients. You are correct that the mechanisms of action was for concentration of intracellular zinc by HCQ acting as an ionophore and in vitro higher levels of zinc prevent viral replications. This was not demonstrated in disease.

Not an off the wall second question. One of the early markers we measure of CoVID infection is D-dimer which is a product of thrombosis and clotting. In virtually all cases there is increased thrombotic activity (and elevated D-dimer) with CoVID infection. We actively anticoagulant many patients with elevated D-dimer to prevent thrombosis. So yes, thrombosis is a very large part of this disease.

Here are some of the interesting questions that are developing around the J&J and AstraZeneca vaccines. Since these vaccines are “more traditional” than the mRNA which is specific for the spike protein, what I think this tells us is that the dead viral particles in these injections still have a highly prothombotic nature, and it tells us a lot about Corona virus 19. From a straight non-political perspective, given that this is not seen with Pfizer and Moderna, I think this means that the thrombosis factors are not in the spike protein but in other regions of the viral genome.

Additionally here is the question that I am really curious about. The J&J was stopped because of 6 cerebral venous thromboses all of which occurred in women. I find it fascinating that there is not any males with this complication. I would be highly interested if these women were on oral contraceptive or other hormonal therapy that synergized with the injection to cause thrombosis. We know that progesterones and exogenous hormones promote thrombosis in young women so is there a correlation between progesterone and thrombosis in CoVID.

The next question I have is if we wish to continue J&J is there a population who would require some low level anticoagulation for a period of time? Then the question is would it be worth it?

Its a very curious outcome and one that bears close watching. I hope this genuinely answers the questions as best as I am able.

I hope you have a pleasant evening and thank you for your asking. I am trying to not be crusty any further — and appreciate your perspectives as well

From a straight non-political perspective, given that this is not seen with Pfizer and Moderna, I think this means that the thrombosis factors are not in the spike protein but in other regions of the viral genome.

Just noticed this.

Let me counter with this suggestion.

https://freerepublic.com/focus/chat/3948996/posts?page=2243#2243

Detailed link on the spike protein (even without furin cleavage site, say, from an mRNA jab) "knocking on ACE2 receptor's door" and this resulting in the cell (by definition, one not subject to lysis as no active virus is involved) sending out a bunch of pro-inflammatory proteins.

I haven't studied the process of inflammation, nor the clotting cascade, so it's a layman's shot in the dark; but do we know of any other consequences of mRNA doing its thing which would send out a bunch of "Hey, let's clot, everybody!" signals throughout the body? Or, alternatively, of other viral proteins which might start a similar inflammatory process?