OspA is one of the outer surface proteins of the Lyme spirochete. There are many of them, labeled A, B, C, etc. So A is pretty important, being the first one. The problem with OspA is that it is a TLR2 agonist. Most TLR2 agonists are fungal, so we refer to them as fungal antigens or fungal-like antigens. Scroll down to the list, here: http://en.m.wikipedia.org/wiki/TLR2.
Fungal antigens ‘tolerize’ the immune cells, so they no longer fight off other fungal antigens. (1, 2) They can also cross-tolerize you to other types of infections. (3) The immune system becomes suppressed and multiple herpesviruses (EBV, CMV, HHV-6 to name a few) can be reactivated. (4) This is known as fungal-viral synergy. Due to the immunosuppression, you may not even produce antibodies to these herpesviruses. You also become susceptible to all kinds of opportunistic infections. The NIH refers to this model as Post Sepsis Syndrome, or “immunoparalysis.”
What do all these ongoing infections do? They screw up mitochondrial function and severely impair the red blood cells’ ability to transfer oxygen, producing fatigue. Chronic EBV is known to cause cancer, MS and other “Great Imitator” diseases.
This mechanism of fungal immunosuppression and virus reactivation is seen over and over…in contaminated vaccines (kids get the illness instead of protection), chronic mold exposure (ME/CFS/Fibro), Gulf War Illness (vaccines & MYCOplasma infection), AND magically revealed with the adverse events from the LYMErix “vaccine,” which was made with Pam3cys–the synthetic version of OspA.
If it hadn’t been intentional, we might be calling it “OopsA.”