Infection with LCMV delays the progression of demyelinating disease in EAE.

Abstract

Abstract Multiple sclerosis is a chronic autoimmune demyelinating disease that affects approximately 2.8 million people worldwide. While several preventative treatments for multiple sclerosis, including Natalizumab and Mitoxantrone exist, there currently is no cure. It is also unknown what provides the initial trigger of disease episodes or exacerbation of the ongoing disease although viral infections might play a role. In contrast to their role as a driver of demyelination, here we investigate whether viral infections play a potential protective role. Using a well-established animal model of chronic-progressive autoimmune disease known as Experimental Autoimmune Encephalomyelitis, we found that infection with lymphocytic choriomeningitis virus (LCMV) infection delayed onset of paralysis as compared to uninfected controls. Consistent with the reduction in EAE disease scores, we identified reduced numbers of myelin-specific CD4 T cells in the CNS. The myelin-specific CD4 T cells were found in the periphery suggesting that the virus impeded their trafficking to the CNS. Additionally, we analyzed that virus-specific CD8 T cells were found in the CNS in preference to the myelin-specific CD4 T cells. Thus, in contrast to the prevailing paradigm of infections driving autoimmune disease progression, we find that viral infection can lessen acute demyelinating disease. R01NS071518 R01AI147641