MHV-68 Induces the Development of Encephalitogenic Disease in an MBP-Specific TCR Transgenic Mouse Model of Multiple Sclerosis
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Date
2022-12
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The Ohio State University
Abstract
Multiple Sclerosis (MS) is a chronic autoimmune demyelinating disease of the central nervous system. While the precise etiology of the disease is unknown, several genetic and environmental factors play a role in the disease's development. Several epidemiological studies have indicated that prior infection with Epstein-Barr Virus (EBV), as well as vitamin D insufficiency, smoking, among other factors are significantly associated with the development of MS. Large seroprevalence studies have indicated a significant correlation between EBV seropositivity and the development of MS. Thus, characterizing how viral infections reshape immune profiles may elucidate pathways that potentiate encephalitogenic disease development. We report that latent infection with MHV-68, an EBV analog, exacerbates autoimmune disease development in a MBP-specific transgenic T cell receptor mouse model. Furthermore, we report that these mice present with MS-like signs previously unreported in EAE models. The purpose of this study was to characterize immunological and transcriptional changes that result from latent MHV-68 infection to further characterize pathways that promote autoimmunity.
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Keywords
Immunology, Autoimmunity, Neuroimmunology, Multiple Sclerosis, Epstein-Barr Virus, MS Pathogenesis