The Epstein-Barr virus (EBV) is a common virus that causes glandular fever (infectious mononucleosis). It has been proposed as a possible trigger for multiple sclerosis,but just having had EBV infection or glandular fever doesn’t mean you will get MS.
EBV, also called human herpesvirus 4, is a very widespread virus. Up to 95% of all adults will have been exposed to EBV, but most of them will not notice any symptoms or ill health. Modern detection methods show that practically everyone with MS has previously had EBV infection. People with EBV antibodies in their blood (showing a previous EBV infection) have a 5.5 times greater risk of MS than those without.
How could EBV affect MS?
EBV can get into the central nervous system, and is present and active in the brain of most cases of MS. It is not yet known whether it produces MS directly or triggers other factors in the immune system that lead to MS. However, given that EBV infection is so widespread, what makes one person with EBV infection go on to develop MS, while another person doesn’t?
This may be where genetic susceptibility comes in, in the form of the HLA system. This is the set of individual markers that your body cells display to protect them from your own immune system. The unique collection of HLA types that you have is called your HLA haplotype.
Some HLA haplotypes appear to make you more susceptible to MS than others. It is possible that this reflects the way in which that haplotype protects against virus infection. Certain HLA haplotypes may allow EBV to spread in the body, and produce more infected cells and antibodies. EBV antibody levels have been shown to be higher in people who later go on to develop MS than those who do not.
A further possibility is that EBV can interact with our own DNA in regions where it is similar to the DNA of the Epstein-Barr virus itself. Our own genomes contain sections of DNA called HERVs (Human Endogenous Retroviruses) which look a lot like viral DNA that has been incorporated into our own DNA millions of years ago. Usually HERVs are benign, but EBV infection may change the way HERVs behave, and influence the immune system in the process. One study showed that increased disease burden and speed of progression of MS was associated with increased activity in HERV regions of the genome.
This association between EBV and the HERV regions of our DNA could suggest new directions for future MS drug research, such as anti-viral therapies.
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