The goal of the VPDS is to help develop means of targeting virus reservoirs and reducing disease progression in people living with HIV. One path toward this goal is to clarify the fundamental biology of HIV persistence during antiretroviral therapy (ART). Motivated by the genetic and functional diversity within key cellular reservoirs for the virus, we are developing high-throughput methods for characterizing large numbers of single cells and viruses in great detail. Topics under investigation include the unique genetic programs expressed by infected cells; heterogeneity among individual infected cells as measured using “omics” tools; and the use of virus genetic analysis to detect critical events that may not be directly observable in vivo. We are investigating these issues both in individuals treated with standard-of-care ART and in study participants receiving experimental HIV cure-directed therapies.
Dr. Boritz began his HIV research career in the mid-1990s as a summer student in the laboratory of Dr. John K. Rose. An interest in fundamental and translational studies of host-virus interactions then led him to pursue combined M.D./Ph.D. training at University of Colorado Health Sciences Center in Denver. He completed his Ph.D. in the Immunology Program studying HIV-specific CD4 T-cell responses with Dr. Cara Wilson. After an internship and residency in Internal Medicine at Johns Hopkins Hospital, he came to NIAID as a fellow in infectious diseases. Following the clinical portion of his fellowship, he joined Dr. Daniel Douek's laboratory at Vaccine Research Center, where he worked to understand the cellular and molecular events that allow HIV reservoirs to persist in vivo. He joined the NIH faculty to establish the VPDS in 2017.
- Ko SH, Bayat Mokhtari E, Mudvari P, Stein S, Stringham CD, Wagner D, Ramelli S, Ramos-Benitez MJ, Strich JR, Davey RT Jr, Zhou T, Misasi J, Kwong PD, Chertow DS, Sullivan NJ, Boritz EA. High-throughput, single-copy sequencing reveals SARS-CoV-2 spike variants coincident with mounting humoral immunity during acute COVID-19. PLoS Pathog. 2021;17(4):e1009431.
- Pérez L, Anderson J, Chipman J, Thorkelson A, Chun TW, Moir S, Haase AT, Douek DC, Schacker TW, Boritz EA. Conflicting evidence for HIV enrichment in CD32+ CD4 T cells. Nature. 2018;561(7723):E9-E16.
- Boritz EA, Darko S, Swaszek L, Wolf G, Wells D, Wu X, Henry AR, Laboune F, Hu J, Ambrozak D, Hughes MS, Hoh R, Casazza JP, Vostal A, Bunis D, Nganou-Makamdop K, Lee JS, Migueles SA, Koup RA, Connors M, Moir S, Schacker T, Maldarelli F, Hughes SH, Deeks SG, Douek DC. Multiple Origins of Virus Persistence during Natural Control of HIV Infection. Cell. 2016;166(4):1004-1015.
- Petrovas C, Ferrando-Martinez S, Gerner MY, Casazza JP, Pegu A, Deleage C, Cooper A, Hataye J, Andrews S, Ambrozak D, Del Río Estrada PM, Boritz E, Paris R, Moysi E, Boswell KL, Ruiz-Mateos E, Vagios I, Leal M, Ablanedo-Terrazas Y, Rivero A, Gonzalez-Hernandez LA, McDermott AB, Moir S, Reyes-Terán G, Docobo F, Pantaleo G, Douek DC, Betts MR, Estes JD, Germain RN, Mascola JR, Koup RA. Follicular CD8 T cells accumulate in HIV infection and can kill infected cells in vitro via bispecific antibodies. Sci Transl Med. 2017;9(373).
- Hiener B, Horsburgh BA, Eden JS, Barton K, Schlub TE, Lee E, von Stockenstrom S, Odevall L, Milush JM, Liegler T, Sinclair E, Hoh R, Boritz EA, Douek D, Fromentin R, Chomont N, Deeks SG, Hecht FM, Palmer S. Identification of Genetically Intact HIV-1 Proviruses in Specific CD4+ T Cells from Effectively Treated Participants. Cell Rep. 2017;21(3):813-822.
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This page was last updated on Tuesday, September 7, 2021