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. PMID: 26727909
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. PMID: 25672885.
Beck SE, Queen SE, Witwer KW, Metcalf Pate KA, Mangus LM, Gama L, Adams RJ, Clements JE, Zink MC, Mankowski JL. Paving the Path to HIV Neurotherapy: Predicting SIV CNS Disease. European J Pharmacology, 2015. Jul 15;759:303-12. PMID: 25818747.