The cause of multiple sclerosis remains elusive, but a preponderance of research indicates that it is a combination of a genetic predisposition and environmental factors. The most promising environmental factor is previous infection with Epstein-Barr virus. Acute infection with this virus in late childhood and early teens results in an infectious mononucleosis. Infection in early childhood is usually asymptomatic. The geographic distribution of MS, i.e., more common in temperate climates, which correlates with the developed world, could be the fact that Epstein-Barr infection occurs in late childhood or early teens in areas where hygiene is better. This would provoke a stronger immune response. Migrants from high-risk to low-risk areas carry the risk if they migrate after approximately the age of 15.
A study in Neurology, March 31, 2015, adds strength to this hypothesis. An Epstein-Barr antigen gene has been identified. MS risk is 5 times greater in people who have anexpression of the 1.2 allele, whereas it is 5 times less likely in those with the 1.3B allele. This finding reinforces the idea that Epstein-Barr virus contributes to disease development.
MS may thus resemble other immune-mediated diseases in which infectious agents are thought to have a key role. For example, strains of enterovirus by infecting pancreatic beta cells may trigger type 1 diabetes mellitus. A norovirus strain contributes to a type of Crohn’s disease seen in mice. Also certain genotypes are known to affect the clinical outcome and the response to therapy of patients with the hepatitis C virus.
It is likely that part of the genetic predisposition to MS is attributed to variants in genes that interact with the Epstein-Barr virus.
Jack Florin, MD
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