Epstein Barr Virus (EBV) has long been implicated in the development of MS.
Professor Sanjay Swaminathan and his team have found that many human genes associated with higher risk of developing MS work with the EBV virus during infection. This might help explain the link between MS and EBV.
Finding out how EBV works together with these human genes could help find ways to control EBV infection and possibly even ways to improve someone’s MS.
Professor Swaminathan’s team has found that one EBV protein hijacks some of the human genes in the cells it infects.
The team have shown that this EBV protein binds more often to particular MS risk genes than it binds to the gene variants associated with MS protection. They were able to successfully block the binding of the EBV protein to the human genes using an inhibitor. They found that this prevented viral “hijacking” of these genes (i.e. stopped the virus from being able to switch these genes on or off). These MS risk genes function in biological processes that are important for EBV growth and function and therefore are likely to affect the survival of EBV immune cells in people.
This work is important because it has shown that MS risk genes make the cell respond differently to hijacking by EBV, and that blocking of this specific viral protein is a potential therapeutic option for targeting EBV in MS. Going forward, the team plans to develop new inhibitors to block this viral molecule using RNA technology, which has been shown in other applications to be safe and effective for therapy in humans.
Finally, there is a marked gender effect in MS, with females significantly more likely to develop MS than males. This phenomenon is likely mediated by sex hormones. Professor Swaminathan’s team has found that some EBV infected immune cells behave differently in males compared to females. They also found that estrogen affected MS risk gene expression and EBV function. These findings suggest that there are gender-specific differences in MS risk gene expression and EBV functions as a result of estrogen. This may in turn contribute to gender differences seen in a person’s response to EBV and to MS susceptibility.
Professor Swaminathan and his team have published several papers based on this work and have presented this work at a national conference.
The team showed that this EBV protein binds human genes associated with MS risk more often than it binds genes associated with MS protection.
This suggests that these human genes might be causing greater risk of MS by changing the body’s response to EBV infection.
Towards developing therapies, the team investigated ways to stop EBV from hijacking human genes during infection.
Using a specific inhibitor, Professor Swaminathan and his team were able to block the EBV protein from binding to the human genes. This stopped the virus from switching human genes on and off. These genes are important for EBV growth and function, so effectively blocking them could help kill EBV.
This work is important because it shows that MS risk genes make cells respond differently to EBV, and that blocking the EBV protein is a potential therapeutic option for targeting EBV in MS.
Going forward, the team plans to develop new inhibitors to block this EBV protein using RNA technology, which can be safe and effective for therapy in humans.
Finally, there is a marked gender effect in MS, with females significantly more likely to develop MS than males. This phenomenon is likely mediated by sex hormones.
Professor Swaminathan’s team found that some EBV infected immune cells behave differently in males compared to females. They also found that oestrogen affects MS risk gene expression and EBV function.
This may contribute to gender differences seen in a person’s response to EBV and in susceptibility to MS.
Professor Swaminathan and his team have published several papers based on this work and have presented this work at a national conference.
Updated: 31 March 2025
$247,400
2020
3 years
Past project
