Neuroglial Infection of Murine-CoV-MHV-A59 Mounts Host Immunity by Regulation of Cellular Stress Response Factors and Antiviral Immune Responses

Padmapriya, S. (2022) Neuroglial Infection of Murine-CoV-MHV-A59 Mounts Host Immunity by Regulation of Cellular Stress Response Factors and Antiviral Immune Responses. Masters thesis, Indian Institute of Science Education and Research Kolkata.

Text (MS dissertation of Padmapriya S, (17MS159)) 17MS159_Thesis_file.pdf - Submitted Version Restricted to Repository staff only Download (1MB)

Abstract

Mouse Hepatitis Virus, MHV-A59 a dual hepato-neurotropic strain of enveloped positive-stranded RNA virus and its isogenic recombinant strain, RSA59 share similar disease etiology. Upon MHV-A59/RSA59 infection in the CNS, major host response factors are activated which causes acute inflammation. Out of many host response elements, oxidative stress induced by ER stress and innate immune responses play the crucial role in elevating the severity of inflammation. When the homeostasis of a cell is disturbed by virus infection, the upregulated oxidative stress responses and innate immune responses function in a positive feedback loop which plays a pivotal role in maintaining the balance between pathogen destruction and protection from tissue injury. Neurons and astrocytes, being the most abundant cells in the CNS and being exposed to a plethora of stimuli from other cells play an important role in balancing the inflammatory responses. In this study, we have analysed the oxidative stress responses and innate immune responses by the neurons (Neuro-2A cells) and primary astrocytes in mounting the host responses towards viral infection which is crucial for maintaining the delicate balance between virus clearance and protection from inflammation mediated tissue damage. We also analysed the changes in the oxidative stress responses and innate immune responses in Neuro-2A cells and astrocytes by modulating the feedback loop with the help of an antioxidant, N-acetyl L-cysteine (NAC). NAC treatment post virus infection in Neuro-2A cells and astrocytes showed decreased viral replication, decreased expression of oxidative stress and innate immune response elements simultaneously.

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