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Master's Student Supervision (2010 - 2020)
Multiple Sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) that causes demyelination of neurons, neurodegeneration and progressive disability. The exact cause of Multiple Sclerosis remains unknown however, susceptibility to MS is influenced by genetics and environmental factors, such as diet. As zero-fiber diets have been associated with exacerbated disease in inflammatory disease models, we investigated dietary fiber’s impact on the murine model of MS, experimental autoimmune encephalomyelitis (EAE). We demonstrated that standard fiber diets (5%) do not offer protection against EAE when compared to zero-fiber diets, whereas a diet high in the soluble fiber, guar gum (30%), inhibited disease progression and prevented lymphocytic CNS infiltration. Other soluble fibers: pectin, resistant starch and inulin did not offer the same protection – providing evidence that the types of dietary fiber have differential effects on the immune system and neuroinflammation.
Mammalian evolution has occurred while hosting mutualistic, commensal, and pathogenic micro- and macro-organisms for millennia. The virome can provide beneficial immune-stimulating signals or it can provide detrimental immune-stimulating signals that impact host health. Mechanisms that are important for relaying signals from the virome to the immune system are not well understood. Here I investigate the importance of a signalling molecule, Signal Transducer and Activator of Transcription-1 (STAT1), in controlling the immune response to an asymptomatic and persistent virus infection by murine Norovirus strain CR6 (CR6). By evaluating clinical parameters and virus-specific adaptive immune responses I was able to better understand how the host can coordinate appropriate immune responses to persistent enteric virus infections. Moreover, I confirmed that host-virome signals could limit CR6 burdens and systemic dissemination in immunosufficient mice. I conclude with a new perspective of how CR6 persists asymptomatically; by therapeutically limiting CR6 replication, I uncovered that unlike other persistent virus infections CR6 persistence may not be due to the apparent weak immune responses against it. Importantly, CR6 persistence requires STAT1 signalling, because deficient signalling leads to uncontrolled virus replication and ultimately host mortality, which limits virus transmission potential