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Man Oh Man's avatar

Thank You Dr. Lee!! I have been following for for a while(Twitter) and believe in your work and appreciate your powerful approach. I didn’t understand at first why your approach was so aggressive until recently and now understand the urgency of your message.

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Biotechnology Student's avatar

Hello Joseph,

I am taking my time here to tell you my thoughts on this and would appreciate an answer from your site.

You are saying that your theory relies on acknowledged facts and that you do not need to do a study that supports your statements. I can completely follow you on your thinking-process that clotting of AB-AG (antibody - antigen) can occur and theoretically lead to long chains/clusters that might lead to blockage in blood/lymph vessels.

However, can you give sources that give insight into the following questions that popped up in my mind:

1] Does a "natural" infection really only result in the production of ONE antibody that is specific for only ONE site of the spike-antigen? Naturally, when the virus is disrupted or virus replication is not completed, I assume that there will be free spike proteins in the blood (with an "open" "bottom site"). So here, antibodies also have the chance to develope against this other site as well.

So is it impossible that in a natural infection, two antibodies types (one against upper, one against lower site) can be produced?

2] Regarding the long AB-AG clusters, do you actually have sources that these can form in a larger scale (more than an oligomere!) in other diseases etc.? And if so - why would they not get "digested" by immune cells? It is an ABs main function to bind to AGs of pathogens and clump the bacteria/viruses together, making them immobile and marking them for digestion by immune cells. So why not here?

To be honest, I have only looked into this specific topic for 3h (but I come from Biotechnology) - I haven't found any papers/textbooks that could answer my questions which instantly came up in my mind.

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