Investigating the host response to chikungunya and respiratory viruses
We are interested in studying the host pathogenesis of viruses such as chikungunya and respiratory viruses with an emphasis on innate immunity. These viruses cause significant mortality and morbidity which demands that we gain a better understanding of their pathogenesis to inform treatment options. Specifically, we focus on how soluble mediators such as type I interferons contribute to host protection, disease tolerance, and/or susceptibility during viral infection. Type I interferons mediate their effects by signaling on target cells to induce downstream outcomes via the induction of hundreds of interferon stimulated genes (ISGs). Recently, we have described how the members of the type I interferons and their ISGs mediate a variety of different effects depending on their timing, location, and disease state of the host. To study these phenomena, we use a variety of tools such as animal models, in vitro cell culture systems, pharmacological agents, genetic deletion mutants, monoclonal antibody technology, and more.
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Every day, our bodies are exposed to pathogens such as viruses and bacteria that have the potential to cause us disease. Most of the time we remain unaware of these threats thanks to our immune system which acts as a defense mechanism to keep our bodies healthy and disease free. However, some pathogens can overwhelm our immune system to cause illness. Upon first contact with a virus such as influenza or SARS-CoV-2, the cells in our body are rapidly made aware of the foreign invader in part by signaling molecules called type I interferons. They are so named because they can interfere with viral infection. These type I interferons signal on our cells to promote activities that fight off the virus. Our lab is interested in understanding the different activities that type I interferons induce to fight off viral infections such as influenza virus that causes “the flu,” Chikungunya virus that causes arthritis, and SARS-CoV-2 that causes COVID-19.
The Lenschow lab is based in the John T. Milliken Department of Medicine and the Division of Rheumatology in the Clinical Sciences Research Building at the Washington University School of Medicine in St. Louis, MO. We are a part of both the Department of Pathology and Immunology as well as the Department of Molecular Microbiology. The principle investigator of the lab is Dr. Deborah Lenschow. Dr. Lenschow completed her M.D., Ph.D. at the University of Chicago studying the role of CTLA4/B7/CD28 co-stimulation in T cell activation and autoimmunity. She then moved to Washington University to complete her medical training and a postdoctoral fellowship with Dr. Skip Virgin where she described ISG15 as an important type I interferon induced, antiviral molecule. Dr. Lenschow opened her lab in 2006 and continues to run an active laboratory focused on type I interferons and interferon stimulated genes during viral infection and autoimmunity.
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