Sumita Bhaduri-McIntosh, M.D., Ph.D.

Sumita Bhaduri-McIntosh, MD, PhDDivision

Infectious Diseases

Academic Title

Associate Professor, Pediatrics and Molecular Genetics and Microbiology
Director, Pediatric Infectious Diseases Research

Contact Information

sbhadurimcintosh@ufl.edu

Training

  • Postdoctoral fellow, Yale University
  • Intern and Resident, Crozer Chester Medical Center, PA
  • Ph.D., Medical College of PA and Hahnemann University, now Drexel University
  • M.B.,B.S., Byramjee Jeejeebhoy Medical College, Pune, India

Research Overview

Sumita Bhaduri-McIntosh is a physician-scientist whose research bridges the fields of Virology, Oncology and Immunology. Research in the Bhaduri laboratory is focused on discovering fundamental biological pathways and understanding cancer development and progression by studying the interaction between Epstein-Barr virus (EBV; a cancer-causing herpesvirus) and its host, the B cell, by investigating two main areas: 1) investigating how EBV subverts anti-pathogen and anti-cancer barriers such as immune responses and the DNA-damage response (DDR) to drive B cell proliferation and transformation, and 2) identifying host factors that determine susceptibility of EBV-infected B cells to lytic activation, a process important for herpesvirus pathology and persistence in humans, and for lymphomagenesis.

In elucidating EBV-host interactions, the Bhaduri lab has made the following fundamental contributions/discoveries:

  • Development of tools to separate EBV-infected lytic and non-lytic cells, a critical step in investigating pathology and persistence of EBV and other herpesviruses
  • The contribution of STAT3 towards maintenance of both cancer-causing human herpesviruses (EBV and KSHV) latency and persistence
  • Antimalarial chloroquine-mediated activation of the EBV lytic phase through chromatin remodeling via ATM,  TRIM28 / KAP1, and KRAB-ZFPs, cellular proteins that cooperate to repair DNA breaks in heterochromatin – relevance to endemic Burkitt lymphoma
  • A new role for STAT3 in regulation of the DNA Damage Response and DNA repair, with broad relevance to cell proliferation and cancer
  • The importance of CD4+ and g-d T cells as well as IgA responses in the context of EBV infection, with implications for EBV-directed adoptive T cell therapies and autoimmune diseases, respectively

About

Dr. Bhaduri is a Pediatric Infectious Diseases specialist with extensive experience in infectious diseases. Specific areas of interest include EBV-lymphomas including EBV-lymphoproliferative diseases in patients with immunocompromise (primary or acquired immunodeficiencies, post-transplant and autoimmune diseases), infectious mononucleosis, chronic active EBV infection, and infections caused by other herpesvirus. Dr. Bhaduri’s clinical expertise influences her research, resulting in identification of novel anti-cancer targets through the use of synthetic lethal approaches, and improving viral oncolytic therapies.

Dr. Bhaduri has had broad training in Infectious Disease research, first as a molecular parasitologist earning her a Ph.D. in Molecular and Cell Biology. As a post-doctoral fellow, she trained as a human cellular immunologist and virologist under the guidance of Professor I. George Miller at Yale. She established an independent research program as an Assistant Professor at Yale followed by a tenured Associate Professorship at Stony Brook University. Dr. Bhaduri has served in a variety of research, clinical, and educational roles and is presently a Children’s Miracle Network Scholar in Pediatric Infectious Diseases.

Key Publications

  1. Li, X., E.M. Burton and S. Bhaduri-McIntosh, 2017. Chloroquine triggers Epstein-Barr virus replication through phosphorylation of KAP1/TRIM28 in Burkitt lymphoma cells. PLoS Pathogens, Epub 2017 Mar 1;13(3):e1006249; doi: 10.1371/journal.ppat.1006249; PMID: 28249048.
  2. Doyle, F., S. Lapsia, S. Spadaro, Z. E. Wurz, S. Bhaduri-McIntosh and S. A. Tenenbaum, 2017. Engineering structurally interacting RNA (sxRNA). Scientific Reports, 7: 45393; PMID: 28350000.
  3. King, C., X. Li and S. Bhaduri-McIntosh, 2015. STAT3 regulates Kaposi’s Sarcoma Herpesvirus lytic activation. J. Virology, 89 (22):11347-11355, Epub 2015 Sept. 2; PMID 26339061.
  4. Koganti, S., C. Clark, J. Zhi, X. Li, E.I. Chen, S. Chakrabortty, E.R. Hill and S. Bhaduri-McIntosh, 2015. Cellular STAT3 functions via PCBP2 to restrain EBV lytic activation in B lymphocytes. J. Virology, 89 (9):5002-5011, Epub 2015 Feb 25; PMID 25717101.
  5. Koganti, S., J. Hui-Yuen, S. McAllister, B. Gardner, F. Grasser, U. Palendira, S. G. Tangye, A. F. Freeman and S. Bhaduri-McIntosh, 2014. STAT3 interrupts ATR-Chk1 signaling to allow oncovirus-mediated cell proliferation. Proc. Natl. Acad. Sci. U.S.A., 111 (13): 4946-4951; doi:10.1073/pnas.1400683111. Epub 2014 Mar 17; PMID 24639502.
  6. Koganti, S., A. de la Paz, A. F. Freeman and S. Bhaduri-McIntosh, 2014. B lymphocytes from patients with hypomorphic mutation in STAT3 resist Epstein-Barr virus-driven cell proliferation. J. Virology, 88 (1): 516-524. Epub 2013 Oct. 30; PMID 24173212.
  7. Hill, E.R., S. Koganti, J. Zhi, C. Megyola, A. F. Freeman, U. Palendira, S. G. Tangye, P. J. Farrell and S. Bhaduri-McIntosh, 2013. Signal Transducer and Activator of Transcription 3 limits Epstein-Barr virus lytic-activation in B lymphocytes. J. Virology, 87(21): 11438-11446; PMID 23966384.
  8. Daigle, D., C. Megyola, L. Gradoville, G. Miller and S. Bhaduri-McIntosh, 2010. Up-regulation of STAT3 Marks Burkitt Lymphoma Cells Refractory to Epstein-Barr Virus Lytic Cycle Induction by HDAC Inhibitors. J. Virology, 84(2): 993-1004; PMID 19889776.
  9. Bhaduri-McIntosh, S.*, M.J. Rotenberg, B. Gardner, M. Robert and G. Miller, 2008. Repertoire and frequency of immune cells reactive to Epstein-Barr virus-derived autologous lymphoblastoid cell lines. Blood, 2008 Feb 1; 111(3):1334-43. Epub 2007 Oct 1; PMID 17942757 *Corresponding author
  10. Bhaduri-McIntosh, S., M. L. Landry, S. Nikiforow, M. Rotenberg, A. El-Guindy and G. Miller, 2007. Serum IgA antibodies to Epstein-Barr virus early lytic antigens are present in primary EBV infection. J. Infect Dis., 195(4):483-92; PMID 17230407.

Complete List of Publications:

http://www.ncbi.nlm.nih.gov/sites/myncbi/1zSwq5mxNBpkI/bibliograpahy/48604975/public/?sort=date&direction=ascending