MIC PDA Members - Short Descriptions

F. Heath Damron, Ph.D. Glomski Lab -- fhd3x@virginia.edu

Elected President of the MIC Postdocs Assiciation
MIC-PDA travel award winner in 2013

My research focuses on Burkholderia cenocepacia and how it uses signal transduction for survival.  B. cenocepacia survives in many niches of the environment as well as in the lungs of cystic fibrosis patients.  Signal transduction systems relay information from the environment to elicit a response.  In particular, I am interested in the post-translational events that activate the RpoE-like alternative sigma factor EcfA.  I wish to identify and characterize the genes and proteins that modulate the activity of EcfA, as well as determine the impact of these on the virulence for the organism.

Mariette Barbier, PhD, Hewlett Lab --  mb6ce@virginia.edu

Elected Vice-President of the MIC Postdocs Association
MIC-PDA travel award winner in 2013

My current research focuses on adapting several protein labeling systems for their use in prokaryotes using a novel protein fusion system. This research will allow the expression of highly versatile tagged proteins that could be used in numerous applications, including basic research and clinical diagnostics. I am also focusing on the creation of promoter fusion vectors that will allow the study of gene expression in in vivomodels of infection.

Ignacio Jundacella, PhD, Ravichandran Lab -- ijj4c@virginia.edu

Engulfment of apoptotic cells by the airway epithelia and how it relates to lung homeostasis.

MIC-PDA travel award winner in 2012

Richard Juneau, PhD, Criss Lab -- raj7q@virginia.edu

Richard received his PhD in Microbiology and Immunology from Wake Forest University in 2011, where he studied neutrophil extracellular trap production in Haemophilusinfluenzae infections.  As a postdoctoral fellow in the Criss lab, he is studying selected bacterial gene products that contribute to N. gonorrhoeae survival after human neutrophil challenge

Yulia Koryakina, PhD, Gioeli Lab - yk6u@virginia.edu

Yulia is studying how the cell cycle regulates AR phosphorylation and transcriptional activity.

MIC-PDA travel award winner in 2012

Thomas Ellison, PhD, Kedes Lab -- tje3x@virginia.edu

Utilizes molecular analysis techniques to study the initial interactions of Kaposi's Sarcoma-associated Herpesvirus with newly infected cells, with a focus on infection of primary human tonsillar cells.

Kunj Pathak, PhD, Engel Lab - kbp9c@virginia.edu

Originally a veterinarian, Kunj received his Ph.D. from University of Kentucky in December 2011. There he used yeast as a model host to understand the roles of cellular proteins, viral RNA and viral replication proteins in the replication of tombusvirus a model positive strand RNA virus. As a postdoc, his research focuses on exploiting yeast to discover new antivirals against Dengue virus

Monika Sharma, PhD, Engel Lab - ms9ef@virginia.edu

The main area of my Ph.D. research was "How host factors are co-opted by the RNA viruses?" I used yeast as a surrogate host to understand the mechanisms by which cellular proteins affect tombusvirus replication. I discovered proteins involved in phospholipid and sterol pathways playing a critical role in replication as well as RNA recombination of tombusvirus. In Engel's lab since July 2012, I am using yeast to discover antivirals against dengue virus. To this end, I am expressing mosquito proteins in yeast and screening a small compound against them.

Evonne Woodson, PhD, Kedes Lab - enj8y@virginia.edu

The initial aim of my project was to characterize the protein components of the Rhesus monkey Rhadinovirus (RRV) purified virion. Earlier work from our laboratory found at least 33 virally-encoded proteins make up the viral particle, but also a subset of cellular proteins including the mitogen-activated protein kinase, ERK2. We found that intravirion ERK2 was phosphorylated/activated and localized to the tegument layer.
In more recent studies, we have been studying the activation of this MAPK/ERK pathway in de novo RRV infection. Our data show that ERK activation is sustained throughout infection through the action of a viral protein product encoded by ORF45. Though similar to the mechanism elucidated in the human homolog, KSHV, our data suggest RRV ORF45 may interact with pERK2 directly, instead of through RSK, to promote its activation as well as the activation of both nuclear and cytoplasmic substrates. We are currently working to determine if pERK2 binding to RRV ORF45, another known tegument protein, serves as a mechanism by which pERK2 is incorporated into viral particles.