Using A549 Cells as a Model for Studying the Ability of Small Molecules to Reverse the Immunopathogenesis of SARS-CoV-2
Advised by Dr. Erin Johnson, Department of Biology
Abstract
COVID-19 has resulted in the deaths of over six million people worldwide. In severe cases of COVID-19, there is a pronounced decrease in the production of interferon-β (IFN-β). INF-β, in the presence of a viral pathogen, elicits the formation of the interferon-stimulated gene factor 3 (ISGF3), which is composed of a phosphorylated signal transducer and activator of transcription 1 and 2 and interferon regulatory factor 9 (STAT1, STAT2, and IRF9). ISGF3 is required to activate the transcription of genes that form the body’s innate antiviral immune response. To date, our lab has identified two compounds, namely KH01 and KH02 that enhance ISGF3 formation and activation in mammalian cells through binding IRF9. This study aims to develop a model for SARS-CoV-2 infection by specifically using A549 airway epithelial cells. If KH compounds can enhance ISGF3 activity in these cells, then IRF9 may be a viable drug target for severe COVID-19.