This explanation holds water to me. Because the spike protein cannot differentiate ACE2 receptors on specific cell types, the spike protein goes everywhere in the body. Additionally, the spike protein is small enough to cross the blood-brain barrier and seems to be negatively affecting the circulatory system. Moreover, the ACE2 protein is a transmembrane protein, meaning that it allows access into the cell if the ligand (spike protein) can provide the key.
I think aggregation of the spike protein is extremely likely, similar to how amyloid plaques in the brain form. I've always been weary of prion diseases becoming a possibility because I didn't find any preliminary results indicating that the spike protein was metabolized back into free amino acids for the body to use.
Perhaps the immune response to the protein aggregates is what is causing the inflammation and other weird effects. Myocarditis?
This explanation holds water to me. Because the spike protein cannot differentiate ACE2 receptors on specific cell types, the spike protein goes everywhere in the body. Additionally, the spike protein is small enough to cross the blood-brain barrier and seems to be negatively affecting the circulatory system. Moreover, the ACE2 protein is a transmembrane protein, meaning that it allows access into the cell if the ligand (spike protein) can provide the key.
I think aggregation of the spike protein is extremely likely, similar to how amyloid plaques in the brain form. I've always been weary of prion diseases becoming a possibility because I didn't find any preliminary results indicating that the spike protein was metabolized back into free amino acids for the body to use.
Perhaps the immune response to the protein aggregates is what is causing the inflammation and other weird effects. Myocarditis?