Molecular mimicry among certain EBV

Molecular mimicry among certain EBV antigens and
certain epitopes of MBP. According to this hypothesis, the primary target of the cellular immune response – that is, some antigens of the EBV – are homologous with certain epitopes of MBP. Owing to this “molecu- lar mimicry,” the cellular immune response against EBV would also involve MBP and therefore, it would be manifested as the autoimmune inflammation of myelin. Although it has been a favorite for long, this hy- pothesis is now considered less convincing because similar cross-reactions exist among the MBP and other viruses – however, a strong epidemiological relation- ship can be demonstrated only with EBV. Therefore, al- though its role cannot be ruled out completely, a cross-reaction itself can hardly be responsible for the relationship between EBV and MS. Most recently, how- ever, Gabibov et al. [34] reported on studies which used a novel approach. They constructed a phage display li- brary of single-chain variable fragments (scFvs) from blood lymphocytes of patients with MS as a potential source of representative MS autoantibodies. Structural alignment of 13 clones selected toward MBP showed high homology within variable regions with cere- brospinal fluid MS-associated antibodies as well as with antibodies toward Epstein–Barr latent membrane pro- tein 1 (LMP1). Accoding to the author, conclusion an- tibodies induced against LMP1 during EBV infection might act as inflammatory trigger by reacting with MBP, suggesting molecular mimicry in the mechanism of MS pathogenesis.
2. Bystander injury hypothesis. The general idea of this hypothesis is that B cells infected by EBV are present also in the CNS and the attack by EBV-specific T cells on the former involves the destruction of surrounding