"Autopsy reports of individuals who died due to SARS show multi-organ dysfunction, with the highest viral titers in the lungs and immune cells in circulation, thus damaging the pulmonary and immune system (45, 46)."
So, the question everybody should be asking is: "How does the virus get into the immune cells?" Yip M.S. [2011] explained it perfectly: "In the presence of anti-spike antibodies, sars-cov readily infects the immune cells via ADE."
That's why the natural immune response focuses on attacking the virus with N-protein antibodies and only uses the S-protein antibodies as a last resort.
There is a logical reason for this. The spike is long and when attached to an anti-body the combination is longer. When an S-protein antibody becomes attached to a virus's spike protein and is then gripped by an immune cell's Fc receptor, the immune cell only gets a "loose" grip of the virus.
The virus effectively becomes tethered to the immune cell and can freely pivot around on the tether. The blood flow combined with the Brownian motion of the water molecules allows the live virus to make contact with the envelope of the immune cell which activates the fusion process allowing the virus to enter the immune cell as an exosome. Exosomes have direct access to the ribosomes and this enables the virus to take control of the immune cell. This totally disrupts the immune response to the virus and causes serious disease.
On the contrary, when an N-protein antibody becomes attached to a virus's envelope and is then gripped by an immune cell's Fc receptor, the immune cell gets a "tight" grip of the virus. The virus cant move and gets digested by the macrophage or encapsulated and processed by the antigen presenting cell. The antigen presenting cell then displays the captured antigen on the MHC-2 molecules for the T-Cells to spot and take action. This process quickly cleans up the virus.
Two different immune attack strategies - two completely different outcomes. Pfizer chose the former. Why? That's a good question?
