spring is released, and the two helices and the loop straighten into one long helix that harpoons the human cell and pulls the virus and human membranes close together until they fuse.” [33]. As Cross explains, through trial and error, but taking structural information into account, researchers came up with the idea of swapping out two adjacent amino acids for prolines in the membrane fusion domain in order to stabilize the shape of the spike protein in its pre-fusion form. In this form, it exposes critical antigenic areas, and this assures more rapid formation of matching antibodies, the only goal of the vaccine design. This also prevents the protein from fusing with the plasma membrane of a host cell. I’d imagine that the spike protein attaches to the ACE2 receptor and then gets stuck there, like a sitting duck. But a worrisome thought is whether this open state, not fused with the membrane, might more closely resemble the shape of a misfolded prion-like protein like amyloid beta than does the collapsed shape it needs to go into the membrane?
Tetz and Tetz have argued in a published online preprint that prion-like domains in the spike protein enable higher affinity for the ACE2 receptor, making the virus more virulent than its earlier cousins [34]. These same authors published an earlier peer-reviewed journal paper where they observed that many other viruses have proteins in their coat that have distinct features of prion proteins [35].
Germinal Centers and Parkinson’s Disease
Germinal centers in the spleen are a primary factory where antibodies against specific antigens (such as the spike protein) are manufactured and perfected. Makers of the mRNA vaccines were pleased to see that antigen-presenting cells (mainly dendritic cells), originally attracted to the site of the injection, take up the mRNA particles and then migrate via the lymph system to the spleen in high numbers and induce high levels of antibody production in these germinal centers [36]. Unfortunately, these same germinal centers are a primary site for the initiation of a process of producing and distributing misfolded prion proteins, often seeded by viral proteins, and triggered by an acute inflammatory response [37].
B cells, also known as B lymphocytes, are a type of immune cell that is the key player in the process that leads to the production of specific antibodies to a foreign antigen [38]. They originate from precursor cells in the bone marrow, and then migrate to the spleen and other lymphoid organs, where they bind to antigens presented to them by antigen-presenting cells, such as the dendritic cells. A maturation process beginning with a multipotent progenitor B cell ends with a mature “memory” B cell that has gone through a complex process to perfect its antibody production process to specifically match the antigen it has been assigned to (e.g., the spike protein).
B cells also go through another process called class switching, which changes the type of antibody they produce from one class to another, without changing its specificity to the antigen. Antibodies are also known as immunoglobulins (Igs), and the possible classes include IgM, IgG, IgA and IgE. IgM is the first immunoglobulin class that is produced (primarily in the spleen), and it is converted into IgG through class switching. IgG is the dominant class in the blood, making up 75% of the serum antibodies, and it is essential for clearing infections in the tissues. Long-lived mature memory B cells cruise the blood stream looking for any appearances of the antigen they have been assigned to, but they are useless for anything else. When the virus they’ve been trained to match mutates to the point where their antibodies no longer match well, they become useless even for the disease they’re trained to fight.
When mice are injected with PrP in the abdomen (intraperitoneal injection), the PrP shows up very quickly in the spleen. From there, the PrP travels along the spinal cord and the vagus nerve to reach the brain, causing prion disease [39]. As we will soon see, α-synuclein, the prion-like protein linked to Parkinson’s disease, also makes its way to the brain from the spleen along the vagus nerve. The mRNA vaccines set up perfect conditions in the spleen for the formation and distribution of conglomerates made up of misfolded α-synuclein, PrP and spike protein.