Interaction between various Epstein-Barr virus traits and the composition of certain genes affects the risk of developing multiple sclerosis (MS), a study reports.
The study, “The interaction of Multiple Sclerosis risk loci with Epstein-Barr virus phenotypes implicates the virus in pathogenesis,” was published in the journal Nature Scientific Reports.
At present, slight variations of the same gene — known as single-nucleotide polymorphisms, or SNPs — at more than 200 gene locations have been linked to a higher risk of developing MS. Most of these genes are particularly active in immune cells.
However, the status of a person’s immune system plays a key role in the real-life effect that a person’s genetics has in MS development.
Previous studies suggest that B-cells (a type of immune cells implicated in MS) infected with the Epstein-Barr virus (EBV, a common form of the herpes virus) contributes to this disease’s onset.
B-cells infected with EBV can become immortalized — a status whereby cells avoid natural cell death and keep proliferating. In the development of MS, immortalized cells escape immune regulation by other immune system cells, leading to attacks on myelin, the protective coating on nerve cells in the central nervous system (brain and spinal cord).
Apart from the presence of EBV-infected B-cells, the number of DNA copies of EBV within B-cells is thought to also influence MS development.
Furthermore, many MS-associated genetic variants (differences in the DNA sequence between individuals) are linked to altered activity in EBV-infected B-cells, supporting evidence of an association between MS and EBV infection.
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