Investigation of the effects of viral infections on certain target genes involved in fibrosis and neurodegenerative disorders

SARS-CoV-2 infection, which emerged in 2019, affects multiple organ systems, primarily the lungs, leading to fibrosis, inflammation, and neurological complications. Similarly, HEV has drawn attention due to its extrahepatic manifestations, particularly its neurological effects. It is estimated that both infections may cause long-term complications through immune-mediated mechanisms. In this thesis study, the expression levels of EMT and fibrosis markers including vimentin, Snail, Slug, E-cadherin, ZEB1, and MAP2K4 were examined in patients with severe COVID-19 and individuals in the recovery phase. The findings demonstrated that fibrotic remodeling and the loss of epithelial barrier function are evident. Furthermore, it was determined that MAPK signaling pathways play a critical role in the processes of fibrosis and inflammation associated with COVID 19. In the second phase of the study, HEV seroprevalence and immune responses were investigated in patients with AD, MS, and PD. Elevated levels of HEV-specific IgG and IgM antibodies, along with HEV-RNA positivity, were detected in these patient groups. It was shown that the expression of IFNB1, ISG15, IRF9, STAT1, and STAT2 genes that play a crucial role in antiviral immunity was significantly suppressed. These results suggest that HEV may exploit the weakened immune response in neurological disorders. Overall, these findings highlight the relationship between EMT and MAPK signaling in the pathogenesis of COVID 19 with related fibrosis and reveal the potential impact of HEV on neurological diseases.