Full Name
Dr. Wael Demian
Job Title
Postdoctoral Fellow
McMaster University
City (Work Address)
State/Province/County (Work Address)
Speaker Bio
Dr. Wael Demian, M.Sc., Ph.D., is a post-doctoral fellow who joined the Mossman laboratory in June 2020. Wael completed his MSc degree (2015) in Memorial University, Nfld. In Memorial University, his MSc work focused on protein analysis using mass spectrometry approaches. Then, he relocated to Toronto to pursue his doctorate degree at University of Toronto. Wael performed his research at Sickkids hospital (PGCRL), and he obtained his Ph.D. (2020) in Biochemistry from University of Toronto. His research interests focused on deciphering signaling mechanisms in cells, mini-organs (organoids), and in intact animals (knockout mice). During his Ph.D., Dr. Demian centred on mTORC1 and the solute carriers (SLC) transmembrane proteins, particularly on the regulation of cell size, proliferation, growth and stress signaling. In the Mossman lab, his postdoctoral studies focus on deciphering signaling mechanisms in human and bats caused by viral infection including (but not limited for) SARS-CoV-2.
Abstract Title
Differential regulation of human and bat IRF3 in response to double-stranded RNA and SARS-CoV-2
Abstract Summary
Interferon regulatory factor 3 (IRF3) is one of the most well-characterized transcription factors involved in the regulation of innate immune responses. Many studies have used IRF3 knockout systems (mice or cells) to analyze the functions of IRF3 in immunity and other biological systems. Understanding mechanisms of IRF3 signaling in taxa that act as viral reservoirs, such as Chiroptera (bats), can identify natural mechanisms of viral suppression in non-human species. In this study, we used RNA-seq to compare human and bat transcriptomic responses to viral infection, and uncovered potential commonalities and differences in antiviral signaling between distantly related mammalian lineages. We simulated viral infection by exposing human and bat (Eptesicus fuscus) cells in vitro to polyinosinic:polycytidylic acid (poly(I:C)), and investigated subsequent interferon and cytokine signaling responses. Further, we interrogated IRF3-independent immune responses by comparing gene expression in vitro in wildtype and IRF3-deficient human and bat cells. Loss of IRF3 dramatically altered global gene expression in human and bat cells following mock and poly(I:C) treatment. Human and bat cells with IRF3 responded similarly to poly(I:C) treatments, while IRF3-deleted bat cells exhibited a unique, IRF3-independent transcriptomic response to poly(I:C) stimulus.
Wael Demian