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Predoctoral Students


Jonathan E. Breitenbach

B.S., Biology, 2002, Louisiana Tech University
Research: The EICP27 protein is an early regulatory protein that acts in concert with other viral proteins to mediate expression of early and late genes of equine herpesvirus 1 (EHV). My research will employ bacterial artificial chromosome and mutagenesis technology to generate a panel of EICP27 mutant viruses. These mutant viruses will be characterized to define the mechanism by which EICP27 functions. Among the questions to be addressed are: Is the EICP27 gene essential for viral replication? What are the relationships Among this protein and the other EHV regulatory proteins?


Crystal W. Burke

B.S., Biology & Biochemistry, 2003, Jacksonville University
Research: Worldwide, the mosquito-vectored alphaviruses are important causes of disease in humans and domestic animals. Interferon induced by virus infection is an important factor in determining the severity of disease in infected hosts. Ms. Wyza is currently investigating the mechanism through which interferon alpha and interferon beta are induced after infection of cells with alphaviruses. Major goals of her research include establishment of an in vitro system in which phosphorylation and nuclear translocation of IRF-3, the primary initial mediator of interferon gene transcription can be accurately measured and subsequently, determination of the specific component of the virus replication cycle that initiates these events.


Robert A. Charvat

B.A., Biology-Chemistry, 2006, Manchester College
Research: Defective interfering particles (DIP) of equine herpesvirus 1 (EHV) are capable of mediating a state of persistent infection.  The DIP genome is comprised of an origin of replication, a cleavage/packaging sequence, and only three genes: UL3, UL4, and a unique gene that is a hybrid of portions of regulatory genes IR4 and UL5.  The goals of this project are to assess the functions of the UL3 and UL4 genes in EHV cytocidal infection and to ascertain if over-expression of UL3 and/or UL4 in the context of the DIP genome contributes to the interference of infectious virus production mediated by DIP.


Carrie B. Coleman

B.S., Biology, 2002, The University of Tennessee at Martin
Research: Gammaherpesviruses cause infections of cells derived from the bone marrow, and are associated with numerous types of malignancies.  Murine gammaherpesvirus 68 (gammaHV68) is genetically related to the human gammaherpesviruses, and provides a small animal model for mechanistic studies of the virus/host relationship in vivo.  We are currently examining the role of infection of B cells and monocytes in the bone marrow, and the effects of this infection on the pathogenesis of viral infection.  We are also defining whether these types of infections alter hematopoietic cell development and function, and determining whether these alterations are involved in the development of lymphoma.


David T. Coleman

B.S., 2006, Microbiology, Mississippi State University
Research: A focus of my work is to characterize the interplay between tumors and their localized microenvironment in the transition of cancer cells to a metastatic phenotype.


Christina L. Gardner

B.S., Biology, 2004, Louisiana Tech University

Research:  My project investigates determinants of Alphavirus virulence and attenuation, focusing on factors that contribute to the virulence of eastern equine encephalitis virus (EEEV) such as cell tropism and resistance to host innate immune responses.  Understanding the factors that contribute to EEEV pathogenesis is important because EEEV is an emerging virus and a potential biowarfare/bioterrorism agent, against which there are currently no licensed vaccines or therapeutics.


Mindy L. Gore

B.S., Biological Sciences, 2004, Louisiana State University and A & M College
Research: The analysis of the roles of the BDLF2 and BMRF2 gene products in infection of B cells and epithelial cells by Epstein-Barr virus.


Shannon M. Kahan

B.S., Microbiology, 2001, Texas A&M University
Research: Murine norovirus shows a tropism for dendritic cells and macrophages in vitro. The focus of my research is to characterize which subsets of cells, within distinctive compartments of the mucosal immune system, are permissive to infection, in vivo, in the presence and absence of type I interferon.

Mary E. Lazarus

M.S., Biology, 2005, The University of Louisiana at Monroe

NEW STUDENT


Roxanne Liles

B.S., Biology, 2004, Northwestern State University of Louisiana
Research: Streptococcus agalactiae (group B Streptococcus; GBS) is a leading cause of sepsis and meningitis in newborns and is an emerging, invasive pathogen of adult populations. Few studies have probed the relationship between in vivo growth requirements and virulence for GBS. Our preliminary studies have identified a putative transcriptional regulator, MtaR, which is required for GBS survival and virulence in vivo. My project objectives are: 1) To identify the MtaR binding site(s) 2) Identify the cis-acting factors within the promoter region of MtaR-dependent genes 3) Identify MtaR effector molecules.


Michael S. Nealy

B.S., Biological Science, 2000, McNeese State University
Research: Gammaherpesviruses cause life-long infections in humans (latency), and are associated with numerous types of malignancies including lymphoma.  Murine gammaherpesvirus 68 (gammaHV68) is genetically related to the human viruses, and provides a small animal model for mechanistic studies of the virus/host relationship in vivo .  We are currently generating mutant viruses to use as tools to dissect the central role of latency in immune evasion and pathogenesis.  The long-term goal of these studies is to better understand the mechanisms by which gammaherpesviruses cause life-long infection and disease.


Maciej T. Nogalski

M.Sc., Chemistry, 2004, University of Warsaw
Research:  A hallmark of HCMV disease is a multiple organ system involvement that stems from the widespread dissemination of the virus within the infected host. Therefore, a critical feature of infection is the hematogenous dissemination of the virus. Our studies have identified that HCMV infects monocytes and induces their extravasation and differentiation into productively infected macrophages. We are currently investigating the HCMV-induced molecular changes in monocytes to better understand how these cells are involved in viral spread and disease.


Krista D. Queen

B.S., Biology, 2006, Louisiana State University - Shreveport
Research: I am investigating Epstein-Barr Virus induced epigenetic alterations in infected carcinoma cells.


Allison M. Repic

B.S., Biology, 2004, Aquinas College
Research: The Epstein-Barr virus latency protein, latent membrane protein 1 (LMP1), is a viral oncogene that can produce both proliferative as well as cytostatic effects on infected cells. We are testing the hypothesis that variable reiterations of the CpG -rich terminal repeats (TR), which are fused in the viral episome and contain the alternate LMP1 promoter, will affect LMP1 expression levels in epithelial cancers. With variable expression levels yielding divergent growth phenotypes, we predict clonal emergence of cells maintaining episomes with an "optimal" TR number.


Kathleen F. Richards
B.S., Biology, 2008, University of North Texas
NEW STUDENT


Joshua J. Steffan

B.S., Environmental Health, 2005, Dickinson State University
Research: The invasion of a tumor into surrounding tissue is a complex multi-stepped phenomenon and determining the factors that promote this process has important clinical relevance. Lysosomes are thought to play a key role by trafficking towards the cellular membrane to release active proteases; allowing tumor cells to degrade and invade into the surrounding stromal tissue. Furthermore, experiments have identified that a growth factor and pH changes can influence this trafficking; thus, a mechanistic understanding of lysosomal trafficking may lead to the development of pharmaceutical inhibitors to block this movement. 


Emily V. Stevenson
B.S., Medical Technology, 2008, Louisiana Tech University
NEW STUDENT


Mulu Z. Tesfay

B.Sc., Plant Sciences, 1998, Alemaya University, M. Sc., Molecular Biology, 2001, Free University of Brussels, M. Sc., Biological Sciences, 2004, Northern Illinois University

Research:  An understanding of the mechanisms through which the innate immune system limits the replication of viruses is an important strategy for development of new antiviral therapies.  Our laboratory has recently discovered a PKR-independent, interferon-induced activity that potently inhibits the genome translation of multiple positive sense RNA viruses.  My project involves characterizing the nature of this antiviral effect and, ultimately, the identification of its effector   protein(s).   


Elizabeth A. Trainor

B.S., Microbiology, 2007, Mississippi State University
Research:  Helicobacter pylori causes a spectrum of diseases, including ulcers, gastritis, and gastric cancer. Factors such as genetics, environmental influences, and diet contribute to the development of disease.  One environmental influence that has not been studied in detail is cholesterol.  The goal of this research is to identify and characterize H. pylori proteins that respond to cholesterol and determine how these proteins affect H. pylori pathogenesis. 


Sarah M. Valencia

B.S., Biology, 2002, The University of Missouri-Kansas City
Research:  Epstein Barr virus infects primarily two cell types B lymphocytes and Epithelial cells.  The purpose of my research is to examine and compare entry and intracellular transport of EBV within these two cell types.


Brittany D. Williams

B.S., Biology, 2007, Louisiana Tech University
Research:  Glioblastoma multiforme is a highly invasive brain tumor and accounts for the majority of brain tumors diagnosed. Patients with gliomas have a very poor prognosis and, unfortunately, have an average survival time of less then a year. My project focuses on the c-Met/HGF signaling axis in promotion of glioma invasion and lysosome trafficking.  Our goal is to discover novel therapeutic targets to inhibit glioma invasion. 

The project described was supported by NIH Grant Number
P20RR018724 from the National Center for Research Resources.

 

 


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