EBV Infection And MS Risk Genes Work Together To Facilitate MS

Epstein Barr Virus or EBV (the virus that causes glandular fever) is a virus that belongs to the herpes virus family and it infects a type of immune cell in the blood known as a B cell. Once a person has been infected with EBV they carry the virus in their B cells for life, meaning their body has to continually control the EBV infection for the rest of their lifetime.

What do we already know about the link between EBV and MS?
Infection with EBV has long been known to be associated with the development of MS. However, while the majority of the population has been infected with the virus (only a small percent will develop recognisable symptoms), 100% of those with MS are thought to be infected.

This shows that while EBV plays a huge role in MS an EBV infection is not sufficient by itself to cause MS. So why do some people who contract EBV develop MS yet others never do? Part of the answer may lie in our genetics.

Previous research funded by MS Research Australia by Professor Michael Pender has shown that people with MS inadequately control these EBV hijacked immune cells and now Australian scientists might have uncovered an interesting interplay between the MS genetic risk factors and EBV.

A new link discovered between EBV and MS risk genes
In a new study, researchers at the Westmead Institute of Medical Research have investigated the way that EBV infection changes which genes the B cells are using and hence changes the way these cells act. Published in Genome Medicine, the researchers compared the gene activity of B cells that were infected with EBV and grown in the laboratory, and cells that had not been infected. They were particularly interested to see whether there would be any changes in the 200+ genetic elements that have already been identified as risk factors for the development of MS.

The research findings explained…
The research showed that a significant proportion of these MS risk genes were influenced by the presence of EBV. This means that:

• The infected cells used the MS risk genes differently in the presence of EBV.
• Some of these genes, in turn, controlled other genes in the cell, meaning there was a domino effect resulting in a number of changes within the cell.
• Further experiments showed that EBV may drive some of these changes at a cellular level through the binding of a molecule called EBNA2. When EBV is hijacking a cell it might try and use a number of cellular genes, and a portion of those are already known as MS risk genes.

This study indicates that the MS risk genes may be working together with EBV infection to facilitate the development of MS and that this interaction may be one way genetic changes act at a biological level to increase the risk of MS.

What do these new findings mean for the future?
A better understanding of the way that EBV infection relates to MS development is important to drive new therapeutic approaches for this disease. Professor Michael Pender’s work has led to the development of a new treatment strategy, currently in clinical trials, based on the idea that boosting a person with MS’s ability to control ongoing EBV infection could help treat MS.

Article courtesy of MS Research Australia