Another interesting story can be found on http://www.msrc.co.uk/
it tells that FTY720 seems to have anti-viral potential - at least in low doses.
Again there may be questions raised regarding an infectious cause of MS...
Just a thought, could it be that immune-system-rebooting (Campath / HDC) acts through killing the infected host-cells of EBV (B-cells) and thereby eliminating the EBV infection, and thus maybe the primary dissease cause?
In this context it might be interesting to see how the HDC following treatment with Copaxone will be doing.
If MS was autoimmune immunetollerance through Copaxone might be important.
If symptoms do return after HDC because of a reinfection with EBV then Copaxone should be without effect - maybe then one could give INF a try for its antiviral properties.
B cells, Epstein Barr Virus and Multiple Sclerosis 12 August 2008
and B Cells
Clonal expansion of B cells and the production of oligoclonal IgG in the brain and cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS) have long been interpreted as circumstantial evidence of the immune-mediated pathogenesis of the disease and suggest a possible infectious cause.
Extensive work on intrathecally produced antibodies has not yet clarified whether they are pathogenetically relevant. Irrespective of antibody specificity, however, the processes of antibody synthesis in the CNS of patients with MS are becoming increasingly clear. Likewise, targeting B cells might be therapeutically relevant in MS and other autoimmune diseases that are deemed to be driven predominantly by T cells.
Accumulating evidence indicates that in MS, similar to rheumatoid arthritis, B cells aggregate into lymphoid-like structures in the target organ. The process of aggregation is mediated through the expression of lymphoid-homing chemokines.
In the brain of a patient with MS, ectopic B-cell follicles preferentially adjoin the pial membrane within the subarachnoid space. Recent findings indicate that substantial numbers of B cells that are infected with Epstein-Barr virus (EBV) accumulate in these intrameningeal follicles and in white matter lesions and are probably the target of a cytotoxic immune response.
These findings, which await confirmation, could be an explanation for the continuous B-cell and T-cell activation in MS, but leave open concerns about the possible pathogenicity of autoantibodies.
Going beyond the antimyelin-antibody dogma, the above data warrant further work on various B-cell-related mechanisms, including investigation of B-cell effector and regulatory functions, definition of the consistency of CNS colonisation by Epstein-Barr virus-infected B cells, and understanding of the mechanisms that underlie the formation and persistence of tertiary lymphoid tissues in patients with MS and other chronic autoimmune diseases (ectopic follicle syndromes). This work will stimulate new and unconventional ways of reasoning about MS pathogenesis.
Source: Lancet Neurology 2008; 7:852-858 © 2008 Elsevier Limited (12/08/08)
Treatment: Gilenya since 01/2011, CCSVI both IJV ballooned 09/2010, Tysabri stopped after 24 Infusions and positive JCV antibody test, after LDN, ABX Wheldon Regime for 1 year.