Immunopathogenesis of viral infections in neurological autoimmune disease

Figures

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  Fig. 1. The mechanism of CMV-induced multiple sclerosis. Immune reaction against the CMV induces autoantibody productions. CMV infection is also associated with a T-cell influx to the CNS, resulting in inflammation. Created with BioRender.com

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  Fig. 2. The mechanism of Epstein-Barr Virus-induced Nervous System damage. EBV life cycle has two phases, including latent phase which provided proliferated viruses without immune reactions. When the number of viruses increased, the immune system reacted against viruses. The EBV-infected B-cells activate which subsequently activate adaptive lymphocytes. The EBV-infected B-cells produce some microRNAs that decrease EBV-specific T-cells and IFN-γ production which resulted in sustained EBV-infected B-cells. Prolonged EBV infections cause changes in the neuroprotective state of microglia to the neurodegenerative state which include neurotoxin production and activation of immune cells. Created with BioRender.com

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  Fig. 3. The mechanism SARS-Cov-2 induces neurological autoimmune system. SARS-Cov-2 enters the nervous system through different receptors. The viruses induce autoimmune reactions through several pathways. 1) The B- cells produce autoreactive antibodies against SARS-Cov-2, which damaged the normal tissues. 2) The recognized virus through PRR induces cytokine storm, resulting in damage to the healthy tissue and new antigens that, releases activate autoreactive T-cells. 3) Subsequently, the T-cell reaction destroys tissues and produce new self-antigens, which induce more autoreactive T-cells reaction. 4) The memory B-cells produce long-term autoantibodies in the absence of virus, which was associated with sustained CNS damage—created with BioRender.com