• Researcher Profile

    Dana H. Gabuzda, MD

     
    Dana H. Gabuzda, MD
     
    Professor of Neurology, Harvard Medical School

    Office phone: 617-632-2154
    Fax: 617-632-4338
    Email: dana_gabuzda@dfci.harvard.edu
    Website: Gabuzda Lab Website

    Preferred contact method: office phone
     
     

    Research Department

    Cancer Immunology and Virology

    Area of Research

    HIV Molecular Biology and Pathogenesis


    Dana-Farber Cancer Institute
    450 Brookline Avenue
    CLS 1010
    Boston, MA 02215

    Biography

    Dr. Gabuzda received her MD from Harvard Medical School in 1983 and did her postgraduate training in internal medicine and neurology at Massachusetts General Hospital. After completing research fellowships at Johns Hopkins University and DFCI, she joined the DFCI faculty in 1991. She is primarily involved in basic laboratory research on HIV replication and disease mechanisms in AIDS.

    Research

    HIV Molecular Biology and Pathogenesis

    The Gabuzda lab uses genetic, biochemical, metabolomic, systems biology, and computational approaches to study HIV infection and comorbidities including cancer. Research interests include understanding viral, host, and environmental factors that determine clinical outcomes, therapeutic responses, and accelerated aging. Current projects include studies on:



    • 1) virus-host interactions during HIV replication and pathogenesis that impact immune control, inflammation, metabolic disorders, and comorbidities

    • 2) role of exosomes in cell-cell communication, immune regulation, stress responses, and disease pathophysiology

    • 3) mechanisms involved in HIV-associated neurological disorders and accelerated aging

    • 4) cancer risk and etiologies in aging populations with HIV


    The lab is proficient at bioinformatic, computational, and systems biology approaches including generation, analysis, interpretation, and visualization of large data sets, big data handling, and using bioinformatic software and R programs for data integration, network prediction, pathway analysis, and modeling. The lab also uses machine learning and other computational approaches to model longitudinal trajectories and identify new predictors of clinical outcomes. The long-term goal is gaining multidisciplinary knowledge that leads to progress in personalized medicine for HIV-infected and aging populations.


    Complete Publications List: http://www.ncbi.nlm.nih.gov/sites/myncbi/dana.gabuzda.1/collections/47703338/public/

    Select Publications

    • Ancuta P, Rao R, Moses A, Mehle A, Shaw SK, Luscinskas FW, Gabuzda D. Fractalkine preferentially mediates arrest and migration of CD16+ monocytes. J Exp Med 2003;197:1701-7.
    • Öhagen A, Devitt A, Kunstman K, Gorry PR, Rose PP, Korber B, Taylor J, Levy R, Murphy RL, Wolinsky SM, Gabuzda D. Genetic and functional analysis of full-length HIV-1 env genes derived from brain and blood of AIDS patients. J Virol 2003;77:12336-45.
    • Mehle A, Strack B, Ancuta P, Zhang C, McPike M, Gabuzda D. Vif overcomes the innate antiviral activity of APOBEC3G by promoting its degradation in the ubiquitin-proteasome pathway. J Biol Chem 2004;279:7792-8.
    • Holm GH, Zhang C, Gorry PR, Peden K, Schols D, De Clercq E, Gabuzda D. Apoptosis of bystander T cells induced by human immunodeficiency virus type 1 with increased envelope/receptor affinity and coreceptor binding site exposure. J Virol 2004;78:4541-51.
    • Wang J, Babcock GJ, Choe H, Farzan M, Sodroski J, Gabuzda D. N-linked glycosylation in the CXCR4 N-terminus inhibits binding to the HIV-1 envelope glycoproteins. Virology 2004;324:140-50.
    • Ancuta P, Moses A, Gabuzda D. Transendothelial migration of CD16+ monocytes in response to fractalkine under constitutive and inflammatory conditions. Immunobiology 2004;209:11-20.
    • Mehle A, Goncalves J, Santa-Marta M, McPike M, Gabuzda D. Phosphorylation of a novel SOCS-box regulates assembly of the HIV-1 Vif-Cul5 complex that promotes APOBEC3G degradation. Genes Dev 2004;18:2861-6.
    • Holm G, Gabuzda D. Distinct mechanisms of CD4+ and CD8+ T cell activation and bystander apoptosis induced by human immunodeficiency virus type 1 virions. J Virol 2005;75:6299-311.
    • Gorry PR, Churchill M, Crowe SM, Cunningham AL, Gabuzda D. Pathogenesis of macrophage tropic HIV-1. Curr HIV Res 2005;3:53-60.
    • *Ancuta P, Kunstman KJ, Autissier P, Zaman T, Stone D, Wolinsky SM, Gabuzda D. CD16+ monocytes exposed to HIV promote highly efficient viral replication upon differentiation into macrophages and interaction with T cells. Virology 2005 (in press).

    Trainees

    • Chettimada, Sukrutha, PhD
    • Dutta, Anuprya, PhD
    • Guha, Debjani, PhD
    • Mukerji, Shibani, MD, PhD
    • Solomon, Isaac, MD, PhD
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