[IlyaMuromec]

There is indeed sound virology that supports the claim that vaccinations cause the very maladies which they are supposed to prevent.
T cells contain a T cell receptor that is like the antibody of B cells. Each T cell has only one kind of receptor. Analogous to the genetic events of antibody production, T cells which contain a T cell receptor that is like the antibody of B cells. Each T cell has only one kind of receptor. Analogous to the genetic events of antibody production, T cells rearrange a set of genes coding for the T cell receptor. Each T cell ends up with a unique receptor, but the population of T cells contains billions of different receptors.
Clonal selection theory illustrates how immunological memory permits a rapid response upon a second exposure to an antigen. Immunological memory is the basis of natural immunity and artificial immunity (i.e., vaccinations).
Each B cell has a specific antibody as a cell surface receptor. The arrangement and generation of antibody genes occurs prior to any exposure to antigen. When a soluble antigen is present, it binds to the antibody on the surface of B cells that have the correct specificity. These B cell clones develop into antibody-producing plasma cells or memory cells. Only B cells, which are antigen-specific, are capable of secreting antibodies.
Following initial exposure to antigen, the plasma cells stop producing antibody and die. Memory cells remain in greater numbers than the initial B cells, allowing the body to quickly respond to a second exposure of that antigen.
The body can make low levels of soluble antibody about one week after exposure to antigen. However, a second exposure to antigen produces a much faster response, and several orders of magnitude higher levels of antibody. The ability of antibody to bind antigen also increases in the secondary response. The memory of antigen and stimulated response is the basis for vaccination.
A secondary immune response (second exposure to an antigen) is not only faster but produces antibody with up to a 10,000 fold increase in binding affinity. This higher affinity comes from a mechanism that alters the variable regions of light and heavy chains of the memory cells by specific somatic mutation. This is a random process that by chance can improve antigen binding.
The system makes one mutation for each two cell divisions. Re-exposure to antigen is most likely to cause clonal expansion of memory cells which produce the highest affinity antibody. The mutations which lead to increased affinity will be clonally selected by antigen similarly to the primary response. Cells with inactive antibody will die by apoptosis from a lack of T cell signaling. Well and good, assuming the vaccine works.
This is quite a two-edged sword here, in the event that a vaccination does not succeed(as many do not), in the event that the antigen is unsuccessful via mutagenesis or whatever reason, then the immune system will have increased the efficacy of the virus by 4 orders of magnitude. Our very own immune system will have, quite efficiently introduced its own version of a potentiator for the virus; depending on the school of virology which one follows, it may be said that we have with our own bodies created quite the cofactor to assist the virus's ability to infect. God may or may not play dice, but with respect to vaccinations, it is a true crap game.
Ilya Muromec