Citation

Multiple Sclerosis (MS) is a chronic, neurodegenerative autoimmune disease of the central nervous system (CNS). The aetiology of the disease remains unknown; however, it is thought to be a combination of environmental factors in genetically susceptible individuals. One such environmental factor is infection with Epstein-Barr virus (EBV), a DNA virus of the gammaherpesvirus family that infects over 95% of individuals worldwide. Following primary infection, EBV establishes a life-long latent infection in the host’s B cells. MS does not develop in the absence of EBV exposure, and EBV is necessary, but insufficient on its own, to cause disease. In a mouse model of EBV and MS, latent infection of mice with ?-herpesvirus-68 (?HV68), the murine homologue of EBV, exacerbates the clinical and immunological outcomes of experimental autoimmune encephalomyelitis (EAE), a common mouse model for MS. The compelling evidence supporting EBV infection as a co-factor in the development of MS has sparked interest in the potential of EBV-targeted therapies to treat the disease, for example by preventing or controlling primary EBV infection using a prophylactic vaccine. As such, mice were vaccinated against, and then challenged with, ?HV68, which successfully reduced the viral load of ?HV68 latent infection. Mice were subsequently induced with EAE. Vaccinated mice displayed an attenuation of viral-enhanced disease, and early in the course of EAE, vaccinated mice displayed significantly reduced CNS immune infiltration compared to unvaccinated mice. This work demonstrates the potential for vaccination against EBV to prevent or ameliorate MS and highlights the urgency and necessity for the development of an EBV vaccine.