Multiple sclerosis (MS) is an immune-mediated disorder; however, little is known about the triggering factors of the abnormal immune response. Different viruses from the herpes family have been mentioned as potential participants. Here, we review the evidences that support the association of varicella zoster virus (VZV) with MS. Epidemiological studies from geographical areas, where incidence of MS has increased in recent decades, pointed out a high frequency of varicella and zoster in the clinical antecedents of MS patients, and also laboratory investigations have found large quantities of DNA from VZV in leucocytes and cerebrospinal fluid of MS patients restricted to the ephemeral period of MS relapse, followed by disappearance of the virus during remission. The above observations and the peculiar features of VZV, mainly characterized by its neurotropism and long periods of latency followed by viral reactivation, support the idea on the participation of VZV in the etiology of MS. However, as with reports from studies with other viruses, particularly Epstein Barr virus, conflicting results on confirmatory studies about the presence of viral gene products in brain tissue indicate the need for further research on the potential participation of VZV in the etiology of MS.
gainsbourg wrote:Once researchers fully explore the hypothesis that herpes sometimes stimulates innapropriate immune response - resulting in nerve tissue damage - I think they will be able to narrow down the area they need to search in order to identify any genes (or congenital disposition) that allow this to happen - and bring about MS. Up till now its been like looking for a needle in a haystack.
Serological evidence of previous exposure to EBV in children with MS supports a role for EBV infection early in MS pathogenesis, as already indicated by prospective studies in adults. Higher antibody titers and T-cell responses to EBV in patients compared to healthy EBV carriers indicate possible continuous viral reactivation, whereas there is some evidence that EBV could break immune tolerance to myelin antigens through molecular mimicry
cellular EBV copy numbers were 3-fold increased in patients with CIDP
gainsbourg wrote:Sometimes CIDP sufferers also get CNS nerve damage (by the way, venous insufficiency has no known link with CIDP).
CVfactor wrote:If MS were autoimmune, it could most likely be initiated by viral influences and I think that molecular mimicry may be a key to this.
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