Sarah E. Beck, DVM, PhD, DACVP
Miller Research Building, Suite 833
Virginia-Maryland Regional College of Veterinary Medicine
Johns Hopkins University School of Medicine
Sarah Beck is a board-certified veterinary anatomic pathologist and veterinary researcher studying primarily CD8 T cell-mediated control of lentiviral infections using animal models. She completed her comparative anatomic pathology residency in the Department of Molecular and Comparative Pathobiology (MCP) at Johns Hopkins University and passed the veterinary anatomic pathology boards in 2014. She also completed her graduate studies in the laboratory of Joseph Mankowski in that same department, successfully defending her thesis entitled, “Immune selection in the CNS: consequences of SIV Gag escape from MHC class I-mediated control” also in 2014. Dr. Beck joined the MCP faculty as an instructor in January 2015 and was promoted to Assistant Professor in January 2016.
Despite the fact that combined antiretroviral therapy is able to control viral replication and prolong the life of Human Immunodeficiency Virus (HIV) infected individuals, HIV remains a pandemic without a cure. Myriad studies have demonstrated that the development of broad, persistent HIV Gag-specific cytotoxic T lymphocyte (CTL) responses plays a major role in control of viral replication and determination of clinical outcome. The primary focus of the Beck lab is studying CTL-mediated immunologic control of viral infections using animal models. Specifically, our current studies are aimed at better understanding HIV Gag-specific CTL-mediated viral control using virus like protein (VLP) vaccination of humanized mice. We hypothesize that vaccination for HIV using this novel VLP platform will stimulate broad HIV Gag-specific cytotoxic T cells, resulting in effective T cell-mediated killing of HIV-infected cells in primary infection, reducing the viral reservoir in HIV-infected BLT mice.
In particular, the Beck lab is interested in exploring cell-mediated immunity (CMI) as an important mechanism for reducing the viral reservoir. Although effective combined antiretroviral therapy (cART) prevents new rounds of HIV infection, it is incapable of eliminating pre-existing infected CD4+ cells, which are the most likely precursors to the majority of latently infected cells. In contrast, CTLs are capable of eliminating either productively infected or non-productively infected cells. Dr. Beck is particularly interested in testing the hypothesis that a boosted HIV Gag-specific CTL response using VLP vaccination in acute infection can reduce or eliminate the viral reservoir.
In addition, as a veterinarian boarded in veterinary anatomic pathology, Dr. Beck also has extensive expertise in infectious disease pathology as well as exposure to a wide variety of laboratory animal models. This includes over eight years of experience interpreting histopathology from numerous animal models of both infectious and neoplastic disease processes using many different species, including (but not limited to): mice, rats, pigtailed and rhesus macaques, rabbits, guinea pigs, chinchillas, New World primates such as marmosets and owl monkeys, African clawed frogs, and zebrafish. This work has included scoring histopathologic lesions on H&E slides, performing necropsies on study animals, performing and interpreting immunohistochemistry, and interpreting immunofluorescence and in situ hybridization assays. Using this expertise, she has collaborated on a number of projects based both at Johns Hopkins and in other universities providing veterinary pathology support.
- Beck SE, Queen SE, Viscidi R, Johnson D, Kent SJ, Adams RJ, Tarwater PM, Mankowski JL. Central nervous system-specific consequences of simian immunodeficiency virus Gag escape from major histocompatibility complex class I-mediated control.. Journal of NeuroVirology, 2016; 22(4): 498-507.
- Beck SE, Kelly KM, Queen SE, Adams RJ, Zink MC, Tarwater PM, Mankowski JL. Macaque Species Susceptibility to Simian Immunodeficiency Virus: Increased Incidence of SIV Central Nervous System Disease in Pigtailed Macaques Versus Rhesus Macaques. Journal of NeuroVirology, 2015; 759:303-12.
- Beck SE, Queen SE, Witwer KW, Metcalf Pate KA, Mangus LM, Gama L, Adams RJ, Clements JE, Christine Zink M, Mankowski JL. Paving the path to HIV neurotherapy: Predicting SIV CNS disease. Eur J Pharmacol. 2015 Jul 15;759:303-12.
Selected Collaboration Publications
- Coleman CM, Sisk JM, Halasz G, Zhong J, Beck SE, Matthews KL, Venkataraman T, Rajagopalan S, Kyratsous CA, Frieman MB.CD8+ T Cells and Macrophages Regulate Pathogenesis in a Mouse Model of Middle East Respiratory Syndrome. J Virol. 2016 Dec 16;91(1).
- Ahidjo BA, Maiga MC, Ihms EA, Maiga M, Ordonez AA, Cheung LS, Beck SE, Andrade BB, Jain S, Bishai WR. The antifibrotic drug pirfenidone promotes pulmonary cavitation and drug resistance in a mouse model of chronic tuberculosis. JCI Insight. 2016 Sep 8;1(14):e86017.
- Feng N, Huke S, Zhu G, Tocchetti CG, Shi S, Aiba T, Kaludercic N, Hoover DB, Beck SE, Mankowski JL, Tomaselli GF, Bers DM, Kass DA, Paolocci N. Constitutive BDNF/TrkB signaling is required for normal cardiac contraction and relaxation.. Proc Natl Acad Sci U S A. 2015 Feb 10;112(6):1880-5.