Wagner Prize

Wagner Prize

Wagner Prize 2014 Award Seminar

Brittany Johnson

Criss Lab
Recipient of the
2014 Robert R. Wagner Prize for Outstanding Research
in Microbiology, Immunology and Cancer Biology

"Neisseria gonorrhoeae phagosome maturation and survival inside primary human neutrophils"

March 19, 2014

1-14 Jordan Hall

Seminar at 4:00 p.m.
Reception to follow



Recipients of the Robert R. Wagner Prize

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2014
Brittany Johnson
Criss Lab

 

M. Brittany Johnson
Ph.D. in Microbiology,  May 2014 (expected date)

Thesis: Mechanisms of Neisseria gonorrhoeae intracellular survival inside primary human neutrophils

Research: Brittany’s thesis research focuses on mechanisms of Neisseria gonorrhoeae (Gc) survival inside primary human neutrophils. Gc is the causative agent of the major global health problem, gonorrhea. In response to infection with Gc abundant neutrophils are recruited. However, Gc can be cultured from patient exudates, indicating Gc has developed mechanisms to defend against neutrophil killing. Brittany made the striking observation that Gc phagosomes avoid fusion with neutrophil primary (azurophilic) granules, allowing the bacteria to remain viable intracellularly. Delayed phagosome-primary granule fusion could be overcome by opsonizing Gc with immunoglobulin or by Gc expression of surface-exposed opacity-associated proteins (Opa). Residence in a degradative phagolysosome resulted in decreased Gc viability by exposing the bacteria to proteases found in primary granules. Together these data reveal that Gc avoids clearance by neutrophils in acute gonorrhea by manipulating neutrophil membrane trafficking to prevent the formation of a degradative phagolysosome.

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2013
Amelia Hufford
Ravichandran Lab

 

Amelia E. Hufford
Ph.D. in Microbiology,  May 2013

Thesis:
"Phosphatidylserine recognition receptors: promoters of muscle development and apoptotic cell engulfment"

Research
In the laboratory of Dr. Kodi Ravichandran, Amelia’s thesis research focused on understanding the role of the phosphatidylserine (PtdSer) receptor, BAI1, and apoptotic cells in muscle development and repair. Myoblasts are muscle progenitor cells that must fuse with one another during muscle development to form multinuclear myofibers. Amelia demonstrated that BAI1 expression in myoblasts positively regulates myoblast fusion, which is dependent on the activation of the ELMO/Dock180/Rac signaling pathway. In vivo, myofibers from Bai1-/- mice are smaller than wild-type littermates, and muscle regeneration after injury was also impaired in Bai1-/- mice, highlighting a role for BAI1 in mammalian myogenesis. Amelia further observed that during myoblast fusion, a fraction of myoblasts undergo apoptosis and expose PtdSer, an established ligand for BAI1. Moreover, she determined that blocking apoptosis potently impairs fusion, and adding back apoptotic myoblasts restores fusion. Finally, primary human myoblasts could be induced to form myotubes by adding apoptotic myoblasts, even under normal growth conditions. Together, these findings identify BAI1 and apoptotic cells as novel promoters of myoblast fusion, with significant implications for muscle development and repair.

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2012
George Liechti
Goldberg Lab

George W. Liechti
Ph.D. in Microbiology, Fall 2012

Thesis:

"Purine acquisition and biosynthesis in Helicobacter pylori"

Research
George works with the bacterium Helicobacter pylori, a causative agent of gastritis, duodenal ulceration, and gastric cancer. He is currently investigating the purine salvage pathway in H. pylori with the goal of fully elucidating the essential enzymes required for maintaining the bacterium’s nucleotide pool. Its inability to synthesize purines de novo makes key enzymes in this pathway attractive drug targets for future antimicrobials.

Matt Hufford, Wagner Prize 2011
2011
Matthew T. Hufford
Braciale Lab

Matthew T. Hufford
Ph.D. in Microbiology, Spring 2011
Thesis:

"Regulation of Cytotoxic T Lymphocytes Effector Function During Experimental Murine Influenza Infection"

Research
Matthew's thesis research focused on the regulation of cytotoxic T lymphocyte (CTL) effector function during murine influenza infection. He demonstrated that indeed CTLs could recognize infected respiratory epithelial cells and destroy the cells but that this T cell/target cell interaction did not lead to release of pro-inflammatory cytokines. By contrast, CTLs also interacted with influenza antigen displaying CD45+ inflammatory cells in the infected lung interstitium. It is this interaction that not only leads to destruction of the cells but to the production of pro-inflammatory cytokines by the CTLs. He further demonstrated that this regulation of T cell effector activity is dependent in part on the presence or absence of co-stimulatory molecules on the targeted cell. These findings have important implications for the development of pulmonary inflammation /injury and "cytokine storm" during severe influenza infection.

Derek Dube. White Lab
2010
Derek Dube
Judy White
Lab

Derek Dube
Ph.D. in Microbiology, Spring 2010
Thesis:

"Ebolavirus Entry: Cell adhesion-dependent control of viral tropism"

Research

In the laboratory of Dr. Judith White, Derek's work has focused on the initial stage of viral entry. Employing cell culture systems, Derek recognized a role for cellular adhesion in the regulation of ebolavirus tropism. He showed that cells that grow in suspension (including lymphocytes) formerly thought to lack an ebolavirus receptor actually sequester a receptor intracellularly, and provided evidence that upon cell adhesion the receptor can be translocated to the cell surface. These results revealed a novel means of regulating viral tropism that is likely of pathological importance for ebolavirus infection. Derek has presented his work at two meetings of the American Society of Virology and, to this point, is the first author on two, and co-author on two, published studies.

Anna Maria Copeland
2009
Anna Maria Copeland
Jay Brown
Lab

Anna Maria Copeland
Ph.D. in Microbiology, May 2009
Thesis:

Herpes Simplex Virus Replication: Roles of Viral Proteins and Nucleoporins in Capsid-Nucleus Attachment.

Research
Replication of herpes simplex virus (HSV-1) involves a step in which a parental capsid docks onto a host nuclear pore complex (NPC). The viral genome then translocates through the nuclear pore into the nucleoplasm where it is transcribed and replicated to propagate infection. We have developed a live cell system to study the interaction between the herpes capsid and the host NPC in the context of an infection. Using the live system, we investigated the roles of viral and cellular proteins in the process of capsid-nucleus attachment. Our results suggest that the viral tegument protein VP1/2 is involved in specific attachment to the NPC and/or in migration of capsids to the nuclear surface. Results indicate cellular Nup358 is required for nuclear capsid binding, possibly serving as the nuclear receptor for herpes capsids. We are currently working to identify a capsid binding domain within Nup358.

2008
2008
Michelle L. Demory
Sarah J. Parsons
Lab

Michelle L. Demory
Ph.D. in Microbiology, May 2008
Thesis:

Investigation of the regulators of epidermal growth factor receptor translocation to the mitochondria and determination of the impact of EGFR association with the mitochondrial protein Cytochrome c Oxidase Subunit II

Research
Our studies utilized a cell model system that mimics late stage breast cancers by co-overexpressing epidermal growth factor receptor and c-Src. We found that EGFR can transiently translocate to the mitochondria where it can associate with the mitochondrial protein cytochrome c oxidase subunit II. Our results suggested this translocation is regulated by a multifaceted regulatory mechanism utilizing clathrin-mediated endocytosis, c-Src and a mitochondria localization sequence. Furthermore, we showed that EGFR can directly phosphorylate CoxII and that EGF stimulation can increase mitochondrial potential and Cox activity.

Laura Adang

2007
Laura Adang
Dean Kedes
Lab

Laura Adang, Ph.D.
Ph.D. in Microbiology, August 2007

Thesis:
Single cell characterization of kaposi's sarcoma-associated herpesvirus infection: tropism, immune evasion, and potential treatments

Research
Lifelong infection is a hallmark of all herpesviruses, and their survival depends on countering host immune defenses. The human γ-herpesvirus Kaposi’s sarcoma-associated herpesvirus (KSHV) encodes an array of proteins that contribute to immune evasion, including Modulator of Immune Recognition 2 (MIR2), an E3 ubiquitin ligase. Our results suggest that the effects of MIR2 are gene dosage dependent and that low levels of this viral protein contributes to the widespread downregulation of immune modulating cell-surface proteins during the initial stages of KSHV infection.

Michael Cruise
2006
Michael W. Cruise
Young Hahn
Lab

Michael Cruise, Ph.D.
Ph.D. in Microbiology, Fall 2005
Thesis:
Enhanced FASL Expression by HCV Core Induces the Production of CXCR3 Chemokines and Liver Damage

Research
Mike was involved in studying Fas/FasL interaction in liver inflammation in hepatitis C virus (HCV) infection. Using transgenic mice expressing the HCV core protein, Mike studied the recruitment of activated T cells to the liver and the mechanism of damage by liver infiltrating lymphocytes. He found that expression of HCV core protein in T cells enhanced the level of FasL. Michael Cruise is currently finishing up his MD degree here at UVa and plans on a residency in pathology.

Antonio DiGiandomenico
2005
Antonio DiGiandomenico
Joanna Goldberg Lab

Antonio DiGiandomenico, Ph.D.
Ph.D. in Microbiology, Fall 2005
Thesis:
Protection from Pseudomonas Aeruginosa Pneumonia After Vaccination with Recombinant Live Attenuated Salmonaella: Correlates of Protective Immunity in the Respiratory Tract

Current Lab
Research Fellow
Vanderbilt University Medical Center
Department of Microbiology & Immunology

Research
My research is focused on the development of recombinant cell penetrating (CP) suppressor of cytokine signaling (SOCS) proteins that can be therapeutically used to inhibit excessive inflammation in a murine model of acute lung injury.
I hypothesize that therapeutic supplementation of intracellular stores of these inhibitory molecules will prevent or lessen the deleterious effects of excessive inflammation in the lung and could have major implications for individuals who are stricken with bacterial pneumonia and suffer unwarranted levels or morbidity.

n. mossamaparast
2004
Nima Mosammaparast
Lucy Pemberton Lab
Nima Mosammaparast, M.D., Ph.D.
Ph.D. in Microbiology, Spring 2005.
Thesis:
Core Histone Nuclear Transport: Mechanisms and links to Chromatin Assembly

Current Lab
Clinical Pathology Resident 2006 to present
Brigham and Womens' Hospital

Research
Nima's research has focused on the molecular mechanism via which distinct nuclear transport factors, also called karyopherins, import chromatin components including histones into the nucleus. He has extended this work to look at how nuclear import may interface with other nuclear processes such as chromatin assembly.

Li Zhang

2003
Li Zhang
Kodi S. Ravichandran Lab

Li Zhang, Ph.D.
Ph.D. in Microbiology, Fall 2004
Thesis:
Genetic studies of Shc function in T cells

Current Lab
Post-doctoral Fellow,
Department of Molecular Biology and Genetics
School of Medicine
Johns Hopkins University

Research
In an attempt to understand the role of Shc during T cell development, so we constructed a conditional transgenic mouse that expresses a dominant-negative (phosphorylation-defective) form of Shc confined to the T cell lineage. After we showed expression of the Shc isoform, we have advanced studies to understand effects on proliferation, differentiation, and even thymic maturation, proving that Shc phosphorylation plays an essential and non-redundant role in T cell development.