Vitamin D (as measured by time of year) and glandular fever are not linked. Should we be surprised?
I guess it boils down to how you think it is all working.
If the month of birth theory holds any water then the major risk period is when you're in the womb or shortly after birth. That the vitamin D hypothesis is also evident in type I diabetes suggests the risk factor is early in life. The biology suggests that vitamin D can shape your immune repertoire (range of different things your immune system responses to). So your die is cast as to whether you are at risk of autoimmunity. But this does not give you autoimmunity. Your other genes also put you at risk.
Whether vitamin D exhibits a major influence once the condition appears, remains to be seen. The trials are being done.
Migration studies from low to high incidence countries suggest you acquire the trigger before you are 15 years for risk of MS. One suggestion is that this trigger is Epstein Barr Virus. This shapes your B cell (antibody making cells) repertoire. Which in turn may determine whether you get MS or other autoimmune conditions associated with EBV.
About half the western population become infected with EBV in infancy. Are these the diabetes-prone people? I guess infection goes unnoticed (undiagnosed) as one of the many episodes of fever that a child has.
In adolescent life the naive/mature B cell gets infected by EBV because the virus enters the B cell via CD21 and an action via HLA-DR. Is this where the number one autoimmune genetic MS risk factor occurs? Is HLA-DRB1*1501 a gene that is good at getting B cells infected by EBV?
The mature B cell is then triggered to proliferate by the virus, and their killing by anti-EBV CD8, cytotoxic T cells cause a cytokine storm and sickness behaviour...that is glandular fever.
The virus causes the B cells to mature into memory B cells and not antibody-producing plasma cells by a protein called EBNA3.
The virus then hides in the memory B cells out of sight of the immune system, but switching off virus production. And as memory B cells are like buses that go round the body, the virus hitches a ride all round the body.
However, the virus does other things, including making the memory B cell independent of the requirement of T cell help. So they do not need to get stimulated by a molecule called CD40. This means, for example, if a memory B cell enters the brain and sees its target it will become activated and so does not need a T cell of the same specificity to be present.
As more damage occurs, more antigens capable of stimulating B cells are liberated. You don't have to postulate that it is one antigen causing the problem and these can change over time. However there is specificity because the B cell would have to see a brain derived signal to trigger release of cytokines to start the lesion.
This would be a great immune-evolution because it makes us more able to fight infection quickly, creating a survival advantage for the human population.
On the down-side, autoimmunity could occur. However, EBV has been with us for thousands of years (co-evolving with us). As humans used to have children earlier in life - and died earlier than we do now - autoimmunity would arguably not be selected against. Why? Because most autoimmunity occurs later in life (old-age and after child birth for our ancestors).
So, evolution-wise, this would not be selected against. Furthermore, even if it did occur in our ancestors, it is at such a low frequency that it does not affect the overall survival of the population.