How EBV might cause immune cells to go rogue in MS
Study shows complex interaction between EBV and MS risk genes.
Last updated: 15th June 2018
- Epstein Barr Virus (EBV) infection can contribute to the development of autoimmune diseases including MS
- The virus can make proteins which bind to DNA and these can interact with the parts of DNA that control MS risk genes
- The variations in some genes that are associated with an increased risk of developing MS are more likely to interact with EBV
Viruses work by evading our bodies’ defences and hijacking our cells. Once inside, they can use our cells to manufacture and copy themselves, or lie dormant until they are ready to move elsewhere
Different human viruses choose to invade different types of cells in the body. The Epstein Barr Virus, which has been linked to the development of MS and some other autoimmune diseases, favours B cells – a type of cell in the immune system.
When viruses commandeer our immune cells, this can cause the cells to “go rogue” and veer off course, which is thought to play a role in the development of autoimmune diseases.
EBV is a very common infection that is most often acquired during early childhood, either without symptoms or as a generic childhood upper respiratory tract infection. In adolescents and young adults, it can also cause glandular fever. Between 90% – 95% of the general population will have been infected by the virus at some point in their life. In comparison, close to 100% of people with MS have been infected. So, it is thought that, on its own, EBV does not cause MS, but, in susceptible people, it contributes to the development of MS. Until now, the exact reason for this was not clear.
When a virus enters a cell, it starts controlling some of the genes in the cell. New research, published in Nature Genetics, has now found that EBV can interact specifically and directly with some of the genes that have been identified as risk genes for MS and other autoimmune disorders.
To show this, the scientists took some cells infected with EBV and some that were not infected. They then worked to identify where proteins from the virus were bound to the DNA of the cells, since this is a key sign that the virus is using those specific genes. In the case of MS, they found that, of the 109 known MS risk genes, the viral proteins were bound to 44 of these genes. Importantly, the virus appeared to do this more readily in B cells than in other cells.
The scientists also looked at whether the specific variations in the DNA code that is linked to MS in these genes changed how strongly the virus proteins bound to the DNA. They found that the virus latched on to the version of the gene code linked to MS more readily than it did to the ‘standard’ version of the gene, suggesting a specific interaction between the MS risk gene variations and EBV.
This work reveals an important mechanism by which our genes and the virus might effectively cause MS only in some people – not everyone – who has been infected with EBV. Ultimately, this type of work may help us to understand how we can prevent the changes that EBV makes to the immune system and help to prevent or treat MS.
With thanks to MS Research Australia – the lead provider of research summaries on our website.