Dina El Bery, Samir A El-Masry, Adel A Guirgis and Dr. Hany Khalil
The highly pathogenic strains of the influenza virus have been responsible for large epidemics and pandemic diseases characterized by severe pulmonary illness connected with high morbidity and mortality rate. Epigenetic reprogramming mechanisms including DNA methylation lead to host immune-related transcriptional programmers' perturbations by regulating chromatin structure and gene expression patterns. Therefore, here we investigated the further changes of DNA methylation in human lung epithelial cells in response to influenza A virus (IAV) infection and figured out how methylation might be activated upon IAV infection. By infecting A549 cells, we found that the expression of DNA methyltransferase 1(DNMT1) and methionine syenthase (MTR) significantly increased according to MOIs of IAV infection 24 hours post infection. Interestingly, the relative gene expression of ten-eleven translocation 1 (TET1), 2, and 3, responsible for DNA demethylation activities, markedly reduced in infected cells reached the lowest expression in the cells infected with MOI of 2 of IAV. Furthermore, unlike interlukine-6 (IL-6), interferon beta (IFN-β) production increased upon IAV infection, while gradually decreasing by 6 hours post infection, indicated by ELISA assay of infected cells. These findings suggested the alteration in DNA methylation process in response to IAV infection proofed by the upregulation of DNMT1 and depletion of TET gene family. This alteration of DNA methylation may affect the cytokine production from infected cells and, subsequently, cellular immune response.
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