• Carrie B. Coleman obtained her B.S. with a concentration in Microbiology at the University of Tennessee at Martin in 2002. As a graduate student she joined the lab of Dr. Scott Tibbetts in the Department of Microbiology & Immunology at LSU Health Sciences Center – Shreveport. Her work in Dr. Tibbetts lab involved utilizing a murine gammaherpesvirus, MHV68, as an in vivo model to characterize the role of developing B cells in the maintenance of viral latency. She obtained her Ph.D. in virology in May 2010 and moved with the Tibbetts’ lab, as a post-doctoral fellow, to the University of Florida were she continued her work to demonstrate that the Bcl-2 homologue encoded by MHV68 blocks B cell receptor-mediated apoptosis and promotes the survival of developing B cells in vivo. In September of 2013 she went on to join the lab of Dr. Rosemary Rochford at SUNY Upstate medical university where her research interests focused on the human gammaherpesvirus, Epsetin-Barr virus (EBV). As a post-doctoral fellow in the Rochford lab she established that the EBV types differ in their cell tropism. EBV type 2, unlike EBV type 1, has a unique tropism for T cells, infecting both B and T lymphocytes. Thus, introduced a new paradigm of EBV-2 cellular tropism, uncovering the potential role of T cells in EBV type 2 latency and disease. When the Rochford lab relocated to the University of Colorado Anschutz Medical Campus in 2015, she moved with the lab, where she collaborated with Dr. Roberta Pelanda and Dr. Julie Lang, directors of the humanized mouse core at UC Denver Anschutz, to develop the first EBV type 2 mouse model, allowing for in vivo studies of EBV type 2. In August of 2019 she joined the department of Microbiology at the University of Alabama Birmingham as an assistant professor to start her own research lab. The broad research interest of her lab is to utilize both in vitro and in vivo assys to understand EBV-2 biology, specifically elucidating the significance of EBV-2 infection of T cells.
  • Selected Publications

    Academic Article

    Year Title Altmetric
    2018 Epstein-Barr Virus Type 2 Infects T Cells and Induces B Cell Lymphomagenesis in Humanized Mice.Journal of Virology.  92. 2018
    2018 A cancer-associated Epstein-Barr virus BZLF1 promoter variant enhances lytic infectionPLoS Pathogens.  14. 2018
    2018 Changes in Tonsil B Cell Phenotypes and EBV Receptor Expression in Children Under 5-Years-OldCytometry Part A.  94:291-301. 2018
    2017 Epstein-Barr Virus Type 2 Infects T Cells in Healthy Kenyan ChildrenJournal of Infectious Diseases.  216:670-677. 2017
    2015 Breast Milk as a Potential Source of Epstein-Barr Virus Transmission Among Infants Living in a Malaria-Endemic Region of KenyaJournal of Infectious Diseases.  212:1735-1742. 2015
    2015 Epstein-Barr Virus Type 2 Latently Infects T Cells, Inducing an Atypical Activation Characterized by Expression of Lymphotactic CytokinesJournal of Virology.  89:2301-2312. 2015
    2014 Virus-Encoded MicroRNAs Facilitate Gammaherpesvirus Latency and Pathogenesis In VivomBio.  5. 2014
    2014 A Gammaherpesvirus Bcl-2 Ortholog Blocks B Cell Receptor-Mediated Apoptosis and Promotes the Survival of Developing B Cells In VivoPLoS Pathogens.  10:e1003916-e1003916. 2014
    2010 Immature and Transitional B Cells Are Latency Reservoirs for a GammaherpesvirusJournal of Virology.  84:13045-13052. 2010
    2010 Use of a Virus-Encoded Enzymatic Marker Reveals that a Stable Fraction of Memory B Cells Expresses Latency-Associated Nuclear Antigen throughout Chronic Gammaherpesvirus InfectionJournal of Virology.  84:7523-7534. 2010

    Research Overview

  • The focus of my research career has been to understand the mechanisms used by oncogenic gammaherpesviruses, to establish and maintain a life-long latent infection. Epstein-Barr virus (EBV) is a human specific oncogenic virus that establishes a life-long latent infection. Significantly, dysregulation of this long-term infection can lead to the development of malignancies, jeopardizing the life of the host. The predominate model of EBV latency, based on studies of EBV type 1 (EBV-1), posits that this virus has evolved to infect B cells and co-opt natural B cell activation pathways, such that infection of naïve B cells results in their activation and subsequent differentiation to memory B cells, where the virus latently resides. My work focuses on expanding this prevailing model. EBV is classified into two types EBV-1 and EBV-2, based on genetic variations. I have shown that the EBV types also differ in cell tropism. EBV-2, unlike EBV-1, has a unique tropism for T cells, infecting both B and T lymphocytes. The infection of T cells resulted in activation, proliferation, as well as alteration of cytokine expression demonstrating that EBV-2 has the ability to modulate normal T cell processes. EBV-2 infection of T cells has been observed in healthy children and in an EBV-2 mouse model, strongly suggesting that infection of T cells is a natural part of the EBV-2 life-cycle. Thus, shifting our view of EBV biology, uncovering the potential role of T cells in EBV-2 latency establishment, persistence, and lymphomagenesis. The broad research interest of the lab is to understand EBV-2 biology, specifically elucidating the significance of EBV-2 infection of T cells and the origins of EBV-2 associated lymphomas.
  • Education And Training

  • Doctor of Philosophy in Microbiology and Immunology, Louisiana State University Health Sciences Center - Shreveport 2011
  • Bachelor of Science or Mathematics in Molecular Biology, University of Tennessee System : Martin 2002
  • Full Name

  • Carrie B. Coleman