Overview
Kenneth W. Witwer is an associate professor of molecular and comparative pathobiology and neurology at the Johns Hopkins University School of Medicine in Baltimore, Maryland, United States. As nominated President-Elect of the International Society for Extracellular Vesicles (ISEV), Witwer previously served as Secretary General and Executive Chair of Science and Meetings of the society. His laboratory studies extracellular vesicles (EVs), noncoding and extracellular RNA (exRNA), and enveloped viruses, including HIV and SARS-CoV-2. Witwer is a member of the Richman Family Precision Medicine Center of Excellence in Alzheimer's Disease, has advised the US Environmental Protection Agency and the US National Institutes of Health, and is an associate editor of the Journal of Extracellular Vesicles.
Career and research
Witwer's PhD dissertation research was on retroviruses and the innate immune system responses to pathogens such as Visna virus and simian immunodeficiency virus (SIV) as models of human immunodeficiency virus (HIV), specifically regulation of microRNAs, cytokines, and the promyelocytic leukemia protein (TRIM19). He then completed a postdoctoral research project on miRNAs as biomarkers of HIV disease. In 2011, Witwer joined the faculty at Johns Hopkins, and he assumed a tenure-track position in 2012. His primary appointment is in the Department of Molecular and Comparative Pathobiology. He has a secondary appointment in Neurology and Neurosurgery. He is a member of the Cellular and Molecular Medicine program and the Richman Family Precision Medicine Center of Excellence in Alzheimer’s Disease at Johns Hopkins.
The Witwer laboratory studies the roles of EVs, exRNA, and ncRNA in HIV disease of the central nervous system and in other neurodegenerative diseases, such as Alzheimer's and Parkinson's. Another focus of the group is on how inflammatory insults like cigarette smoking affect progression of disease. Beginning in 2013, Witwer examined the hypothesis that RNAs such as miRNAs in dietary substances could regulate endogenous genes in mammals. These studies led him and others to the conclusion that this type of regulation is unlikely to occur in normal physiology.
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