Michael S. Diamond, MD, PhD
The Herbert S. Gasser Professor, Departments of Medicine, Molecular Microbiology, Pathology & Immunology
- Associate Director, Center for Human Immunology and Immunotherapy Programs
- BA, Political Science: Columbia College of Columbia University, New York, NY (1985)
- PhD: Cell and Developmental Biology, Graduate School of Arts and Sciences, Harvard University, Boston, MA (1994)
- Medical Degree: Harvard Medical School, Harvard University, Boston, MA (1994)
- Research Fellowship, Molecular and Cell Biology: University of California, Berkeley, CA (1995)
- Residency, Internal Medicine: University of California, San Francisco, CA (1997)
- Clinical Fellowship, Infectious Disease: University of California, San Francisco, CA (1998)
- Research Fellowship, Department of Public Health, Infectious Disease Unit: University of California, Berkeley, CA (2001)
- Infectious Disease
- Internal Medicine
Research in the Diamond laboratory focuses on the interface between viral pathogenesis and the host immune response. For several years, we have been primarily focused on two globally important mosquito-borne human pathogens, West Nile virus and Dengue virus. Both are single-stranded positive-sense RNA viruses of the same genus (flavivirus) that cause human disease worldwide. Recently, we have begun to study other emerging viral infections including Zika and Chikungunya viruses as well as new bunyaviruses. We are interested in defining mechanisms of innate immune restriction and viral immune evasion, generating novel mouse models and understanding the epitope specificity of protective antibodies. In addition, our studies also now focus on the use of high throughput CRISPR/Cas9 whole genome screens to identify host factors required for these viral infections.
Studies with viruses have focused on investigating their pathogenesis and the immune system response that controls infection. Using in vitro models of infection in primary neurons, macrophages, and dendritic cells, we are studying the mechanisms by which viruses causes direct injury to specific target cell types, and how the host responds to limit viral replication. Using mouse models we have defined critical roles for interferon, novel interferon stimulated genes, antibody, complement, CD4+ and CD8+ cells in the control and eradication of flavivirus infection and have begun defining how the microbiome modulates these phenotypes. We also study the structural and molecular bases of antibody-mediated protection of flaviviruses and alphaviruses, with a goal of identifying broadly neutralizing antibodies and their respective epitopes.