“As you know I think EBV causes MS, i.e. I think it is the pivotal factor in the causal pathway that leads to the onset of the disease. Studies have consistently shown that the immune response to EBNA-1 (EBV associated nuclear antigen-1) is increased in people at risk of MS and/or who have MS. Please note the use of ‘and/or’, because most people develop biological disease, i.e. MS, before their first symptoms. EBNA-1 is a so called latency programme antigen and keeps the EBV genome in hibernation. Some feel EBNA-1 is a molecular mimic and triggers cross-reactive immune responses to self-proteins. This is one of the main EBV hypotheses. Another hypothesis is that EBV infects cells within the brain and spinal cord and hence stimulates immune responses, by up-regulating innate immune mechanisms, or danger signals. If EBV does infect the central nervous system you would expect the nervous system to be enriched for T-cells reactive against EBNA-1. The small study below suggests that is the case. However, it does not show a difference between MS and other inflammatory conditions. Maybe this study is just detecting CD8+ T-cells that are prostitutes?”
Erdura et al. EBNA1 antigen-specific CD8 + T cells in cerebrospinal fluid of patients with multiple sclerosis. Journal of Neuroimmunology. Available online 19 March 2016 – In Press.
Epidemiological data suggests that Epstein–Barr virus may be involved in the pathogenesis of Multiple Sclerosis (MS). We aimed to determine the frequency of CD8 +T cells specific for one EBNA1-derived epitope (HPVGEADYFEY) in cerebrospinal fluid (CSF) and blood of patients with MS and other inflammatory neurological diseases (OIND). The frequency of specific CD8 + T cells was assessed by HLA-class-I-binding pentamers restricted to HLA-B35. The frequency of HPVGEADYFEY-specific CD8 + T cells did neither differ significantly in blood nor CSF in MS compared to OIND, but was consistently higher in CSF compared to blood regardless of diagnosis.