Amy L. Hartman, PhD

Amy Hartman Research Manager, RBL
Assistant Professor

Infectious Disease & Microbiology
9014 BST3
3501 Fifth Avenue
Pittsburgh, Pennsylvania 15261

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Phone: (412) 648-8765
Fax: (412) 648-8917
E-mail: hartman2@cvr.pitt.edu
Webpage: http://www.publichealth.pitt.edu/home/directory/amy-l-hartman
Lab Information

Phone: (412) 648-1922
Fax:
E-mail:
Webpage:
Lab Members:
      • Caroline, Amy L
      • Hartman, Amy Lynn

Biography

      Dr. Hartman received her bachelor's degree in Biology from Washington and Jefferson College in 1998. She received her Ph.D. in Molecular Virology from the Department of Molecular Genetics and Biochemistry at the University of Pittsburgh School of Medicine in 2003. Her graduate thesis was done in the laboratory of Mickey Murphey-Corb, Ph.D. and focused on host factors controlling Simian Immunodeficiency Virus (SIV) infection in rhesus macaques. Amy then did a post-doctoral fellowship in the Special Pathogens Branch at the Centers for Disease Control and Prevention in Atlanta, GA under Stuart Nichol, Ph.D. Her work focused on viral virulence factors contributing to severe disease induced by infection with Ebola Zaire virus. Amy returned to the University of Pittsburgh in 2007 as the Research Manager of the Regional Biocontainment Laboratory with a primary faculty appointment in the Department of Infectious Disease and Microbiology (IDM) in the Graduate School of Public Health (GSPH).

Research

      Dr. Hartman's broad research interests center on understanding the pathogenic mechanisms of RNA viruses, particularly arboviruses (viruses transmitted by insect vectors). Rift Valley Fever virus (RVFV) is a mosquito-borne virus that causes severe disease in livestock and humans in Africa and the Arabian peninsula. Rift Valley Fever is found endemically in these regions, and rainfall alterations can lead to epizootics in livestock and epidemics in humans. RVFV is easily transmitted when humans handle infected animal carcasses, and this transmission is thought to be by mucosal exposure or direct inhalation of virus particles. Due to its ability to infect by the aerosol route, RVFV is also considered a potential bioterror threat. For these reasons, better vaccines and therapeutics for this globally-important emerging infectious disease are needed. Current research projects in Dr. Hartman's lab focus on developing animal models for RVFV after aerosol infection. With funding from the Department of Defense, the goal is to develop animal models that mimic the different disease outcomes seen in humans after RVFV infection. Dr. Hartman has established the first well-characterized animal models of the neurological disease that is seen in some RVFV-infected people. These animal models are currently being used to understand how the virus causes lethal encephalitis. Dr. Hartman's animal models have also been used to test novel antiviral drugs, such as Favipiravir (T-705), to determine its broad-spectrum applicability to treat emerging diseases. In addition to her work with RVFV, Dr. Hartman is also interested in developing animal models for other highly pathogenic arboviruses. Well-defined disease models are critical for testing potential vaccines and therapeutics that can be used to protect the US military and civilian populations. Dr. Hartman's lab at the University of Pittsburgh Regional Biocontainment Laboratory has the necessary federal approvals to work at BSL-3, advanced equipment, and trained staff to successfully implement large research grants and contracts aimed at understanding the pathogenesis of infectious diseases.

Selected Publications

  • Caroline, A.L., D.S. Powell, L.M. Bethel, T.D. Oury, D.S. Reed, and A.L. Hartman. 2014. Broad spectrum antiviral activity of Favipiravir (T-705): Protection from highly lethal inhalational Rift Valley Fever. PLOS Neglected Tropical Diseases. 8(4): e2790. doi: 10.1371/journal.pntd.0002790


  • Hartman, A.L., Powell, D.S., Bethel, L.M., Caroline, A.L., Schmid, R.J., Oury, T., and Reed, D.S. 2014. Aerosolized Rift Valley Fever virus causes fatal encephalitis in African green monkeys and common marmosets. Journal of Virology 88(4):2235-2245. DOI: 10.1128/JVI.02341-13.


  • Powell, D.S., R.C. Walker, D.T. Heflin, D. Fisher, J.B. Kosky, L.C. Homer, D.S. Reed, K.S. Cole, A.M. Trichel, and A.L. Hartman. In Press. Development of novel mechanisms for housing, handling, and remote monitoring of common marmosets at animal biosafety level 3. Pathogens & Disease. DOI: 10.1111/2049-632X.12140. PMID: 24453160.


  • Reed, D.S., Bethel, L.M., Powell, D.S., Hartman, A.L. In Press. Differences in aerosolization of Rift Valley Fever virus resulting from choice of inhalation exposure chamber: implications for animal challenge studies. Pathogens & Disease.


  • Bales, J.M., D.S. Powell, L.M. Bethel, D.S. Reed, and A.L. Hartman. Choice of inbred rat strain impacts lethality and disease course after respiratory infection with Rift Valley Fever Virus. 2012. Frontiers in Cellular Infection Microbiology. 2(105):1-14.


  • Bird BH, Githinji JW, Macharia JM, Kasiiti JL, Muriithi RM, Gacheru SG, Musaa JO, Towner JS, Reeder SA, Oliver JB, Stevens TL, Erickson BR, Morgan LT, Khristova ML, Hartman AL, Comer JA, Rollin PE, Ksiazek TG, Nichol ST. Multiple virus lineages sharing recent common ancestry were associated with a Large Rift Valley fever outbreak among livestock in Kenya during 2006-2007. J Virol. 2008 Nov;82(22):11152-66. Epub 2008 Sep 10. PMID:18786992


  • Hartman AL, Ling L, Nichol ST, Hibberd ML. Whole-genome expression profiling reveals that inhibition of host innate immune response pathways by Ebola virus can be reversed by a single amino acid change in the VP35 protein. J Virol. 2008 Jun;82(11):5348-58. Epub 2008 Mar 19. PMID:18353943


  • Hartman AL, Bird BH, Towner JS, Antoniadou ZA, Zaki SR, Nichol ST. Inhibition of IRF-3 activation by VP35 is critical for the high level of virulence of ebola virus. J Virol. 2008 Mar;82(6):2699-704. Epub 2008 Jan 16. PMID:18199658


  • Bird BH, Albariño CG, Hartman AL, Erickson BR, Ksiazek TG, Nichol ST. Rift valley fever virus lacking the NSs and NSm genes is highly attenuated, confers protective immunity from virulent virus challenge, and allows for differential identification of infected and vaccinated animals. J Virol. 2008 Mar;82(6):2681-91. Epub 2008 Jan 16. PMID:18199647


  • Hartman AL, Dover JE, Towner JS, Nichol ST. 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. 2006 Jul;80(13):6430-40. PMID:16775331





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