Excessive inflammation triggered by a hitherto undescribed mechanism is a hallmark of severe SARS-CoV-2 infections and is associated with enhanced pathogenicity and mortality. 88% of COVID-19 patients illustrate metabolic iron changes during infection with SARS-CoV-2. Our groups have long-standing expertise in studying in detail infectious diseases and hostpathogen interactions taking into account the complement system. Further, the Wilflingseder lab has established a primary, human pseudostratified 3D respiratory epithelial/immune model over the last years. This model is very versatile, since innate and adaptive components of the immune system can be easily added. During the last year, the Weiss and Wilflingseder labs successfully expanded novel variants of SARS-CoV-2 patient isolates and worked on various projects resulting in high impact publications on SARS-CoV-2 interactions and therapeutic interventions (Posch et al., 2021a, b, c; Lafon et al., 2021). My task is to do research on deregulated host iron homeostasis, involvement of complement in SARS-CoV-2-mediated type I IFN response of infected tissues and on the connection of iron homeostasis, host metabolism, innate antiviral immune responses and complement functionality. State-of-the-art methods will be used (multi-parameter flow cytometry, high content screening, multiplex PCR). To tackle this complex task with an important translational impact
about
faculty members
students
dates
publications
application
news
innsbruck
contact
