John C. Boothroyd

Stanford University


Primary Section: 44, Microbial Biology
Secondary Section: 61, Animal, Nutritional, and Applied Microbial Sciences
Membership Type: Member (elected 2016)

Biosketch

John Boothroyd, PhD, is the Burt and Marion Avery Professor in the Department of Microbiology and Immunology at Stanford University School of Medicine. He received his BSc from McGill University in Montreal, Canada, and his PhD in Molecular Biology from Edinburgh University in Scotland. Prior to joining the Stanford faculty in 1982, he worked as a scientist in the Immunochemistry and Molecular Biology Department at Wellcome Research Laboratories, UK. In addition to his research role, Dr. Boothroyd has served as Chair of the Department of Microbiology and Immunology, Senior Associate Dean for Research and Training, and is currently Associate Vice Provost for Graduate Education at Stanford. He is passionate about the importance of effective mentoring and the legacy that one’s trainees represent. In 2008, he received the Leuckart Medal from the German Society for Parasitology and in 2016 he was elected to the U.S. National Academy of Sciences.

Research Interests

Dr. Boothroyd is fascinated by the interaction of an infectious agent and the host it infects. His entry into this field came with his joining a collaborative effort to understand antigenic variation in Trypanosoma brucei, the causative agent of African Sleeping Sickness. His group went on to co-discover mRNA trans-splicing and polycistronic transcription in these single-celled eukaryotes. For about the past 25 years, he and his collaborators have been immersed in studying the pathogenesis of another single-celled eukaryote, Toxoplasma gondii. Unlike the African trypanosomes, this ubiquitous cousin of the malaria parasite, Plasmodium, can only grow within another cell. His current work is focused on asking: (1) how Toxoplasma invades and co-opts almost any cell type from almost any warm-blooded animal; (2) how the parasite persists in the human host; 3) how it introduces a collection of polymorphic “effectors” into a host cell; and 4) how these varied effectors produce different disease severity in the host, ranging from asymptomatic to fatal.

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