An array of environmental risk factors for MS have been examined over the past century. Of those, the Epstein-Barr virus (EBV), ultra-violet light exposure and vitamin D levels, and cigarette smoking have the clearest supporting evidence (Wingerchuk, 2011).
The evidence concerning the relationship between MS and MBV isn’t conclusive, however. And these studies have been countered by other studies (Willis et al, 2009; Peferoen et al, 2010; Sargsyan et al, 2010). To read the argument in support of EBV being a requisite causative agent in the pathogenesis of MS, click here; to read the argument against EBV being a requisite causative agent in MS pathogenesis, click here.
In 2010 an international team led by U.-C. Meier (Tzartos et al, 2012) identified clues that may help explain how the Epstein-Barr virus might contribute to the brain inflammation that occurs in MS. White matter postmortem MS tissue and control tissue were analyzed for the expression of the proinflammatory cytokine interferon α (IFNα) by immunohistochemistry, and for EBV by using EBV-encoded RNA (EBER) in situ hybridization. They found high levels of interferon alpha in active MS brain lesions, as well as neighboring immune B cells latently infected by Epstein-Barr virus, in the absence of active viral infection. These findings may point to a possible mechanism for how the virus might indirectly stimulate MS disease activity.