As I understand it, CCSVI is not in contradiction with the previous immune/autoimmune theory, it dovetails nicely with it. There was always the missing piece of the puzzle for why the immune reaction begins in MS and how the leukocytes get into the CNS when the blood brain barrier should keep them out in large numbers. CCSVI may be a promoter of the condition of MS as it is already understood. With the very high association with MS that has been shown and the possible effect on blood flow to the organs most affected in MS (brain and spine), I consider it very much worth supporting research into CCSVI.
You have just pointed out why it is a dangerous things to do to an 'MS' patient, to give them Tysabri. Its mechanism of action is to prevent leukocytes from crossing the blood-brain barrier, when it has been breached by some unknown mechanism, or, as we now know, by CCSVI. If they are prevented from entering the CNS compartment, when normally at least they, could cross into it, they are prevented from keeping PML (and who knows what other pathogens?) in check. The auto-immune hypothesis has been proven by this drug to be a deadly 'theory'. Other drugs somehow induce leukemia, though one could speculate that a condition involving angiogenesis might have something to do with that as well (do they cause leukemia in healthy controls?).
If, as we now know, there is no auto-immune condition causing hyper-immunity, some 'MS' patients might have *hypo*-immunity, and be prime targets for PML. Especially those who have had immune modification by Interferon or chemotherapy, or even steroids.