Kate D. Ryman, PhD
Microbiology and Molecular Genetics
3501 Fifth Avenue
Pittsburgh, Pennsylvania 15261
Phone: (412) 624-3667
Fax: (412) 624-4440
Phone: (412) 624-4482
Ander, Stephanie Elaine
Buchan, Gregory James
Gardner, Christina L
Girardi, Jenna M
Kubica, Patrick Lawrence
Maksin, Chelsea L
Ryman, Kate D
Trobaugh, Derek W
Watson, Alan M
Weiss, Christopher Michael
Dr. Ryman recently relocated to the University of Pittsburgh as an Associate Professor in the Department of Microbiology and Molecular Genetics. She received her B.S. degree in Microbiology from the University of Surrey, Guildford, U.K. As part of the degree program, she worked at Ciba-Geigy (now Novartis) in England for a year and then in Switzerland after graduation. In 1991, she began her Ph.D. studies in the laboratory of Dr. Alan Barrett at the University of Surrey, and moved to the University of Texas Medical Branch in Galveston, TX when Dr. Barrett's lab relocated. She was awarded a Ph.D. degree in Virology by the University of Surrey in 1995. Afterward, she became a postdoctoral fellow with Dr. Robert Johnston at the University of North Carolina-Chapel Hill (UNC-CH), where she gained extensive experience and expertise in the study of immunological and molecular aspects of mosquito-borne virus pathogenesis and disease. She was promoted to Research Assistant Professor at UNC-CH in 2000 and then, in 2002, joined the faculty of the Department of Microbiology & Immunology at Louisiana State University Health Sciences Center in Shreveport, LA. In 2004, she was the recipient of the Charles Randall Lectureship awarded by the South Central Branch of the American Society for Microbiology for “Outstanding Accomplishments in Microbiology.”
Dr. Ryman's laboratory studies enveloped RNA viruses from the families Flaviviridae and Togaviridae, many of which are classified as potential agents of biowarfare/bioterrorism and emerging infectious disease by NIH/NIAID and/or CDC because they are highly pathogenic in humans, but typically there are no effective antivirals or licensed vaccines available. The specific focus is on developing a better understanding of the way in which the early virus-host interaction shapes the outcome of infection. As understanding of the host-pathogen interaction increases, it will be possible to rationally design antiviral drugs for acute phase therapy and live attenuated virus strains that can be used as vaccines.
- Gardner, C.L., G.D. Ebel, K.D. Ryman and W.B. Klimstra. (2011). Heparan sulfate binding by natural eastern equine encephalitis viruses promotes neurovirulence. Proc Natl Acad Sci USA, 108:16026-31.
- Gardner, C.L. and K.D. Ryman. (2010). Yellow Fever: A reemerging threat. Clinical Laboratory Medicine, 30:237-260.
- Meier. K.C., C.L. Gardner, M.V. Khoretonenko, W.B. Klimstra and K.D. Ryman. (2009). A mouse model for viscerotropic disease caused by yellow fever virus infection. PLoS Pathogens, 5(10):e1000614.
- Gardner, C.L., J. Yin, C.W. Burke, W.B. Klimstra and K.D. Ryman. (2009). Type I interferon induction is correlated with attenuation of a South American eastern equine encephalitis virus strain in mice. Virology, 390:338-347.
- Yin, J., C.L. Gardner, C.W. Burke, K.D. Ryman and W.B. Klimstra. (2009). Similarities and differences in antagonism of neuron alpha/beta interferon responses by Venezuelan equine and Sindbis alphaviruses. Journal of Virology, 83:10036-47.
- Gardner, C.L., C.W. Burke, M.Z. Tesfay, P.J. Glass, W.B. Klimstra and K.D. Ryman. (2008). Eastern and Venezuelan equine encephalitis viruses differ in their infectivity for dendritic cells and macrophages: Impact of altered cell tropism on pathogenesis. Journal of Virology, 82:10634-10646.
- Tesfay, M.Z., J. Yin, C.L. Gardner, M.V. Khoretonenko, N. Korneeva, R.E. Rhoads, K. D. Ryman and W.B. Klimstra. (2008). Interferon alpha/beta inhibits cap-dependent translation of viral but not cellular mRNA by a PKR-independent mechanism. Journal of Virology, 82:2620-2630.
- Ryman, K.D., C.L. Gardner, K.C. Meier, C.A. Biron, R.E. Johnston and W.B. Klimstra. (2007). Early restriction of Alphavirus replication and dissemination contributes to age-dependent attenuation of systemic hyperinflammatory disease. Journal of General Virology, 88:518-529.
- Ryman, K.D., K.C. Meier, C.L. Gardner and W.B. Klimstra. (2007). Non-pathogenic Sindbis virus causes hemorrhagic fever in the absence of alpha/beta and gamma interferons. Virology, 368:273-285.