Are you vaccinated?

The binding of antibodies still occurs (in many cases if not all) well below the cellular level.
Many use three amino acids  in the foreign protein.
Protein folding means the set of three may NOT be directly adjacent in the actual molecule.
This is one of the things that makes identifying autoimmune reactions.

We are reasonably confidential that Epstein Barr (the virus that also triggers infectious mononucleosis,
and is the initial trigger for MS anti-myelin antibodies).

But what set of proteins? in what arrangement , especially after folding.
And why only in certain people?
Epstein Barr is ubiquitous in humans.
Estimates of its presence in humans have ranged up to (95% or higher).
Yet only a very small phenotype develop MS.
And the phenotype appears to be loosely genetically coupled.
There is a familial presence of MS.
If you have it, there is an increased rate among you direct brothers and sisters.
With a looser coupling to cousins.

This is a question of why does he look different than me? Different alleles of the same gene lead to theoretically predictable differences in clonal selection, and then random AID-related events during the memory pathway lead to further, theoretically unpredictable differences in specificity.

1. Pleomorphism in the MHC class II and III genes resulting in differences in B-cell selection. Pleomorphisms in complement C2 and factor B (closely-related MHC class III molecules important in the classical and alternative pathways, respectively) can produce up to 10000-fold differences in antigen uptake, and of course, pleomorphisms in MHC class II (mainly HLA-DP,DQ,DR) can lead to differences in antigen presentation. Thus, the amplitude of a response (and thus what we perceive as differences among individuals) is dictated by these events which control antigen uptake and presentation.

2. AID (the B-cell specific, activation-induced cytosine deaminase) leading to less predictable specific differences among individuals. So, after B-cell clonal selection, clonal expansion occurs and the first wave of B-cells give rise to 1) IgM-producing plasma cells (terminally differentiated cells, so committed to secreting soluble antibody that they lack the surface expression of BCR and CD40, and programmed for eventual death); and 2) to B-cells on the memory pathway. B-cells on the memory pathway can undergo class switch recombination (IgA1-2, IgG1-4, IgE), dependent upon what type of T-cell help they receive. If committed to the memory pathway, B-cells may undergo AID-related changes by generating different specificities as a result of (1) somatic hypermutation, (2) class-switch recombination, or (3) "templated mutations" with a VH-region pseudogene. AID is dependent on ssDNA, which occurs in all three processes.

As an aside, most antigen recognition is mainly primary structure (sequence or how the subunits are linked) recognition (like phone numbers). And only immunoglobulins (not the TCR or MHC class I or II) really see tertiary, secondary, and quaternary structure. Even most antibodies are mainly specific for primary sequence.

Yes.