The problem I see with with this theory: If the immune system responds to the vaccine, it produces maybe 200 different antibodies against the spike protein of the virus. If the immune system fights the whole virus, it produces the same antibodies and some thousand different antibodies more against the rest of the virus. So how could it be that the subset of antibodies is more dangerous than the full package? An if the virus can produce antibodies that help him to invade the body, why don't we see many reinfections?
we were told that this COVID-19 virus had the exact same spike proteins as HIV
No, the spike protein is the part that binds to the cell, this is unique in SARS-CoV-2. Some Indian scientists told us that they have found sequences of the HIV in the payload of SARS-CoV-2. But we would have heard more of it if it had been reproducible.
https://www.biorxiv.org/content/10.1101/2020.01.30.927871v1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7141560/
Perhaps not identical, but I still find this striking, although I'm not a virologist. I am happy to be corrected. I was not aware of the Indian researcher's claim; I was never referring to the core genome of the virus, as I was unaware that claim had been made.
To your first question, I simply don't know. I don't know what the mRNA sequence in the vaccine is encoding, so I don't know the nature of the epitope that is going to be presented, or whether that's to target antibody formation against spike proteins, or what. Some of your language confused me a bit, as far as the virus producing antibodies. The issue with the ADE scenario is that the antibodies our WBCs produce are actually acting as vectors for the virus to basically live cryptically within the immune cells, evading elimination.
As far as the information I had been originally commenting on, I also don't know the mechanism which causes the increased TH2 type response. Could it be ADE influencing that? Sure.
bioRxiv papers are interesting if they are fresh, but after some time a peer reviewed publication should follow, otherwise there is something wrong with them. The bioRxiv paper is interesting because it shows a way to do such research for yourself: Download RNA sequences from open source databases and compare them with open source software. If you find a large chunk of virus A inserted into virus B, there is maybe a story behind it. If the chunk is large enough, you can use some statistical magic to proof that this could not happen by accident. In this case, it seems the statistical magic of the authors were not convincing enough to get a peer review, so the paper has been withdrawn by its authors.
The paper from 2004 is about SARS version 1.0. If it is valid for version 2.0 too, there should exist a more recent paper.
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