Elucidating the mechanistic role of latent EBV infection in the etiology of MS
Year Awarded: 2017
Term: 3 years
Funding Amount: $354,048
Affiliation(s): University of British Columbia
Province(s): British Columbia
Researcher(s): Dr. Marc Horwitz
Research Priorities: Cause of MS
Impact Goal(s): Prevent MS
- Research suggests that Epstein- Barr virus (EBV), the causative agent of mononucleosis, is a potential trigger of multiple sclerosis (MS).
- The mechanisms regulating MS in individuals infected by EBV is unknown.
- The research team will:
- Investigate the immune response in animals with MS-like disease, previously infected with EBV.
- Identify cellular pathways involved in EBV-induced triggers of MS.
Epstein-Barr virus (EBV), best known as the cause of infectious mononucleosis (mono), is believed to play a role in the cause of MS. The risk of developing MS is 10 times greater in individuals infected with EBV during childhood, and 20 times greater in those who have developed mononucleosis. In his previous grant, also funded by the MS Society, Dr. Mark Horwitz identified that mice infected with an EBV-like virus developed a disease highly reminiscent of MS which includes a severe disease course, infiltration of immune cells into the brain and spinal cord, and demyelination. His current project builds on these findings to further examine the mechanisms regulating MS in mice with MS-like disease that were infected with EBV-like virus. Specifically, he will investigate the immune response following EBV induced-infection to discover cellular and molecular pathways, understand the unique geographic/age-related association with MS incidence, and translate the findings in mice to observations in individuals with MS. The ultimate goal of Dr. Horwitz’s project is to refine therapeutics to interrupt these specific EBV-immune interactions and prevent MS.
Potential Impact: The results from this study could be important in the development or refinement of therapeutics to interrupt EBV and immune system interactions and prevent MS.