Innate and Intrinsic Host Enzymes Shaping RNA Virus Infection
Michaela Gack, PhD
Scientific Director
Arthur and Marylin Levitt Endowed Chair
Cleveland Clinic Florida Research and Innovation Center
Dr. Gack is the Arthur and Marylin Levitt Endowed Chair and Scientific Director of the Cleveland Clinic Florida Research and Innovation Center. She did her PhD training in virology at Harvard Medical School as part of a collaborative graduate program between Harvard and the Friedrich Alexander University (FAU) Erlangen-Nuremberg, Germany. Before joining Cleveland Clinic in 2020, she held faculty positions at Harvard University and The University of Chicago.
For her academic achievements in the fields of virology and innate immunity, Dr. Gack received several awards including the GE & Science Prize for Young Life Scientists, the Robert Koch Postdoctoral Prize, the Ann Palmenberg Junior Investigator Award from the American Society for Virology, and the Merck Irving S. Sigal Memorial Award of the American Society for Microbiology. She has also been selected twice on Germany’s list of “Top 40 under 40” scientists. In 2017, she was awarded the Vilcek Prize for Creative Promise in Biomedical Science, and in 2021 she received an NIH Director’s PIONEER Award. Dr. Gack has continuously served on National Institutes of Health study sections and also as an editor for a number of journals including Journal of Virology and PLOS Pathogens. She is currently serving as an editor for Human Molecular Genetics and is also a member of the editorial board of Science Signaling.
Summary
Host cellular enzymes such as kinases, phosphatases, and ubiquitin E3 ligases have been shown to play critical roles in orchestrating antiviral defense programs, such as cytokine (e.g. interferon) responses and autophagy. Moreover, some of these enzymes directly target viral components inducing their degradation or modulating protein activity. A major group of E3 ligases that restrict RNA virus and DNA virus infections is the TRIM (tripartite motif) family of proteins, with >70 members encoded in the human genome. In turn, many viruses antagonize specific TRIM proteins in order to sustain their successful replication in the host. In this talk, I will present our recent work on how host cellular enzymes of the TRIM protein family restrict virus infections and the influence these activities have on viral disease outcome.
Learning Objectives:
- Define the role of different innate and intrinsic antiviral pathways (i.e., cytokine responses, autophagy, direct virus restriction) in immune defense
- Explain the different mechanisms by which TRIM E3 ligases modulate virus infection and viral disease outcome
This page was last updated on Tuesday, March 17, 2026