September 6, 2019  Print

A new study, led by The Westmead Institute for Medical Research (WIMR), indicates that a flawed immune response to the Epstein-Barr virus (EBV) can potentially increase the risk of multiple sclerosis (MS).

Dr Grant Parnell and Professor David Booth were involved with the study. 

This finding suggests that therapies that target EBV could be beneficial in halting or slowing the progression of MS.

The study, published in Genome Medicine, used Genome-wide Association Studies (GWAS) to provide genetic evidence that EBV can facilitate the development and progression of MS.  GWAS is a relatively new way for scientists to search the genome (the complete set of genes in a cell) for gene variations that occur more frequently in people who have a particular disease. It helps pinpoint genes that might contribute to an increased risk of developing that disease. It also identifies how EBV interacts with the human immune system and identifies a molecular mechanism to control disease, targeting an EBV gene.

EBV is a member of the herpes family. It’s perhaps best known for causing glandular fever, although it is also thought to be involved in a number of cancers and immune disorders, including lupus, rheumatoid arthritis, Sjögren’s syndrome and MS.  Most people are infected with EBV during their lifetime, but it shows no effect because the immune system responds by limiting or preventing it from spreading. 
Professor David Booth, head of the Immunogenetics Group at The Westmead Institute for Medical Research and lead researcher for the study says that, while EBV is necessary for the development of MS, it is not sufficient to cause it alone.

“Our new study indicates that the way a B cell (a type of immune cell) responds when it is first penetrated by EBV can contribute to MS susceptibility. However it is not the lone cause.  It is, in fact, one of a growing list of risks,” said Professor Booth.

The study indicates that many of the genetic risk factors for MS that have been identified using GWAS are associated with the way the immune system responds to the infection.

Professor Booth added, “Genes that affect MS susceptibility do so by participating in the processes that leads to an irregular, or flawed immune response.  If these processes are ongoing, they can drive the development of MS.  Therefore, reversing these processes is likely to halt progression.”

Professor Booth says that while this study provides strong evidence about how EBV and the immune response it triggers is involved in the development and progression of MS, a lot more research is needed.

“But reducing EBV infection through the molecular processes identified in this paper should be helpful in treating MS.  Work to achieve this is ongoing at WIMR and elsewhere.”

Professor David Booth is affiliated with Sydney University and The Westmead Institute for Medical Research.
This study was supported by the NHMRC, MS Research Australia, Juvenile Diabetes Research Foundation, and Macquarie Group Foundation.