Great post and here is another thought to add to the works:
RESULTS: Serological evidence for remote EBV infection was present in 83% of pediatric MS patients compared with 42% of emergency department and healthy controls (P<.001). Five pediatric MS patients were negative for all 3 EBV antigens. Pediatric MS patients were less likely than controls to have been exposed to herpes simplex virus (P =.003), while seropositivity for cytomegalovirus, parvovirus B19, and varicella zoster did not differ between MS patients and controls. CONCLUSION: These results suggest an association between EBV infection and pediatric MS
From the pediatric MS study on relationship to ebv. based on this,
it appears that MS is not 100% associated with EBV as was suggested by the other paper. Clearly since kids (God bless them) are the youngest persons with MS, unless we believe it to be a different disease, their profile should be the least impacted by other factors and later infections and thus the most pure data. Of course MS could be several diseases
But one other thing that is true is that once one has had EBV the b cells are infected and carry it for life. This paper was on serological evidence not CSF so my comment here may seem immaterial but as other papers point out the EBV presence in CSF I'd like to point out that it may be possible that the "MS process" whatever it is brings thusly ebv infected b cells into the CNS and thus causes the apparent issue of CNS infection.
I have RA and there was excitement about EBV being causal in that arena some years back as it was present in the joints of people with RA very frequently and not in healthy joints . Since b cells are infected for life once one has EBV, b cell presence in joints with active immune involvement was eventually thought to be the cause of the presence of the ebv in the joints rather than causal of the RA.
Back on to the brain, activated microglia "invite" b cells into the CNS
Despite what appears to be a marvelous strategy for keeping microbes out of the brain parenchyma, when looked at from the perspective of the large number of viruses, bacteria, fungi, parasites, and proteinacious pathogens that are "neurotropic," i.e., that have a predilection for infecting the nervous system (Table 3), the brain could be considered an "immunologically underprivileged" organ. Thus, an evolving concept of microglia is that when it comes to defense of the CNS against invading microorganisms, they do not function on their own but rely on their ability to "call in the troops," i.e. lymphocytes, monocytes, and neutrophils
from this terrific review on microglia here http://cmr.asm.org/cgi/content/full/17/ ... _Microglia
My bias is that CPn or another stealth pathogen like Lyme is a plausible cause in MS and therefore ebv presence is not at all unexpected as a secondary phenomenon since it causes lifelong infection of the b cells. in my view it is possible that the microglia, activated by apoptosis of oligodendrocytes caused by Lipopolysaccharide (LPS) presence which is secondry to death of a gram negative bacteria like chlamydia pneumoniae, call in the troops of the peripheral nervous system to help clean up the mess and thus ebv is brought along by the b cells entering in response. You could then culture the ebv in the CNS in much higher numbers than in healthy people.
Even if you believe the autoimmune idea then the presence of b cells in the CNS means that an ebv infected person will have ebv in the cns.
It is a very complex issue