Amy (Seman) Hartman, PhD
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Program:
Molecular Virology and Microbiology
Graduated:
8/2003
Mentor:
Dr. Michael Murphey-Corb
Thesis:
Simian Immunodeficiency Virus (SIV) Production From Rhesus Macaque CD4+ T T Lymphoctes In Vitro: Insights Into the Host Factors Controlling the Rate of Progression to AIDS In Vivo
Previous Institutions Attended:
Washington and Jefferson College, BA in Biology and Spanish
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I am an ORISE Post-doctoral fellow within the Molecular Biology Section of the Special Pathogens Branch (SPB), Division of Viral and Rickettsial Diseases, CDC. The Special Pathogens Branch is dedicated to diagnostics and research on the world’s deadliest RNA viruses. We deal with many virus families, including Filoviruses (Ebola, Marburg), Bunyaviruses (Rift Valley Fever, Crimean-Congo Hemorrhagic Fever, etc), Arenaviruses (Lassa Fever, Machupo, Junin, LCMV, etc), and Coronaviruses (SARS). The Molecular Biology section of SPB performs routine diagnostic testing using real-time Taqman PCR on samples sent to CDC from around the world. In addition, the section does basic molecular biology and pathogenesis research on diseases like Ebola and Rift Valley Fever. The majority of work performed within SPB is done within the high-containment BSL-4 laboratory.
My work since arriving at CDC 3 years ago has concentrated on using reverse genetics to study the pathogenesis of Ebola Hemorrhagic Fever. Because Ebola virus causes such a rapid and severe disease, early events after viral infection may be critical in determining the levels of viral replication and outcome of infected patients. I study the VP35 protein of Ebola, which has been shown to antagonize the Type I Interferon system of the host cell. My initial work mapped the IFN-antagonism domain of VP35. Subsequently, I have been using a reverse genetics system to engineer mutations into recombinant Ebola viruses with the idea of testing the effect of VP35 mutations on virus replication in vitro and on pathogenesis in an animal model.
In addition to my basic research project, I was involved in the outbreak of Marburg Hemorrhagic Fever in Angola in 2005. Upon receipt of samples of suspected hemorrhagic fever patients from Angola, SPB’s routine diagnostic PCR assay identified the agent as Marburg virus. As part of a team of 5 scientists from SPB, I traveled to Luanda, Angola in May 2005 to establish and run a diagnostic laboratory in the local hospital. We established a high-containment laboratory to process patient samples and then used our real-time Taqman PCR assay to analyze samples for the presence of Marburg virus. High titers of virus were found in blood, serum, nasal swabs, oral swabs, and breast milk from suspected patients. This experience in Angola really emphasized for me the connection between basic research and public health.
Recent Publications:
Hartman, A. L., J. E. Dover, J. S. Towner, and S. T. Nichol. 2006. Reverse genetic generation of recombinant Zaire Ebola viruses containing disrupted IRF-3 inhibitory domains results in attenuated virus growth in vitro and higher levels of IRF-3 activation without inhibiting viral transcription or replication. J Virol. 80(13):6430-40.
Towner, J. S., M. L. Khristova, M. Vincent, T. K. Sealy, B. R. Erickson, D. Bawiec,
A. L. Hartman, A. Comer, S. Zaki, H. Feldmann, P. Rollin, T. G. Ksiazek, and S. T. Nichol. 2006. Emergence of Marburg Virus in Angola, West Africa. J Virol. 80(13):6497-516.
Hartman, A. L., J. S. Towner, and S. T. Nichol. 2004. A C-terminal basic amino acid
motif of Zaire ebolavirus VP35 is essential for type I interferon antagonism and displays high identity with the RNA-binding domain of another interferon antagonist, the NS1 protein of influenza A virus. Virology. 328:177-184.
Publications while a graduate student at Pitt:
Kinchington, P.R., Fite, K, Seman, A., and S.E. Turse. 2001. The Virion Association of IE62, the Varicella Zoster Virus (VZV) Major Transcriptional Regulatory Protein, requires expression of the VZV Open Reading Frame 66 Protein Kinase. Journal of Virology 75:9106-9113.
Seman, A.L., W. F. Pewen, L. F. Fresh, L. N. Martin, and M. Murphey-Corb. 2000. The replicative capacity of rhesus macaque peripheral blood mononuclear cells for simian immunodeficiency virus in vitro is predictive of the rate of disease progression in vivo. Journal of General Virology 81:2441-2449.
What were some of the most positive and surprising things about living in Pittsburgh? Being a native Pittsburgher, I initially did not want to stay in the area for graduate school. However, after interviewing at a number of other universities, I saw first hand that Pitt really measured up and exceeded what I saw at other big-name institutions. Through a series of interviews, I realized the faculty at Pitt was top-notch. Faculty members were encouraging and supportive of all the graduate students, which gave Pitt a different feel from other schools I visited. In addition, the students were happy and content. Pitt exceeded my expectations for graduate school.
As for the city of Pittsburgh itself, I thought it was a great place to go to graduate school. The school is easily accessible from local neighborhoods by public transportation. While the city is small, it is large enough to have a decent social live and activities outside school. What did you enjoy most about your research experiences and graduate studies here at Pitt? The other students and faculty members that I got to know during my studies at Pitt have had a tremendous impact on my career. I enjoyed the close family feel that the graduate program had.
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