25/04/2025
Person centered Health means stepping away from the medical model and broadening the therapeutic approach "the role of pathogens in the development of autoimmune disease, and now with MS and EBV we have strong proof that the mechanism of molecular mimicry is no longer just a theory. Since EBV persists in the body, there is now a clear rationale for antiviral herbs in patients with MS."
Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system (CNS), which is linked to Epstein-Barr virus (EBV) infection preceding the disease. The molecular mechanisms underlying this connection are only partially understood, but there is now strong evidence that infection with EBV is a necessary step in the disease development. A research group previously described molecular mimicry between the EBV transcription factor EBV nuclear antigen 1 (EBNA1) and three human CNS proteins: anoctamin-2 (ANO2), alpha-B crystallin (CRYAB), and glial cellular adhesion molecule (GlialCAM). Molecular mimicry is a mechanism where a foreign antigen (say from a virus or bacterium) has a structure or sequence that closely resembles a self-antigen (on a protein of the body). This can trigger the immune system to mistakenly attack the self-tissue in an attempt to eliminate the pathogen and thereby cause ongoing tissue damage.
Now these scientists have strongly supported the clinical relevance of their initial finding by investigating antibody responses against EBNA1 and GlialCAM in a large cohort of 650 MS patients and 661 matched population controls, and compared these to responses against CRYAB and ANO2. They confirmed that elevated IgG responses against EBNA1 and all three CNS-mimic antigens are associated with an increased MS risk. Their findings also showed that higher levels of specific antibodies against EBNA1 and these brain proteins were linked to a greater risk of developing MS.
Additionally, it was shown that MS patients carrying a particular genetic risk factor (HLA-DRB1*15:01) had increased antibody responses against these proteins, and the combination of this genetic risk factor with specific antibodies further raises the risk of MS. The researchers concluded that, overall, molecular mimicry between EBNA1 and GlialCAM is likely an important mechanism contributing to MS pathology.
For several decades I have been advocating the role of pathogens in the development of autoimmune disease, and now with MS and EBV we have strong proof that the mechanism of molecular mimicry is no longer just a theory. Since EBV persists in the body, there is now a clear rationale for antiviral herbs in patients with MS.
For more information see: https://pubmed.ncbi.nlm.nih.gov/40063790/
