The Stephanie and Richard Vogel Graduate Student Award

This endowed award, in memory of Anne DeStefano Nucci and Elidio John Nucci, was established in 2010 and provides support for graduate students enrolled in the College of Computer, Mathematical, and Natural Sciences that study host responses to infectious agents.  The award allows a scholastically excellent student to focus entirely on their Ph.D. research toward the end of their graduate training. 

2016-17 Awardees

Sarah Ahlbrand (MOCB, Briken Lab)


According to the CDC, tuberculosis is considered to be one of the greatest killers due to an infectious agent worldwide and causes millions of deaths each year.  My research focuses on understanding the molecular biology behind how Mycobacterium tuberculosis, the bacteria that causes tuberculosis in humans, evades the host immune response to cause disease.  More specifically, I’m interested in understanding how M. tuberculosis prevents secretion and signaling of cytokines by cells.  Cytokines are proteins that are produced and secreted by our immune cells to signal to other, nearby cells and direct the immune response.  Both our lab and other labs have shown that M. tuberculosis has evolved ways to manipulate and control cytokine secretion so that it can avoid being detected and targeted by other immune cells.  By understanding the molecular biology behind this phenomenon, we can hopefully discover new drug targets that could lead to the development of more effective therapeutics.

2015-16 Awardees

Steve Christensen (MOCB, Mosser Lab)

Leishmaniasis, a disfiguring and potentially fatal disease prevalent in tropical areas, affects over one million people each year. My research aims to study the interaction between the disease-causing parasite (Leishmania) and the cells that it infects (macrophages). Due to 20+ species of the parasite and the population's genetic diversity, presentation of disease ranges from skin lesions to systemic manifestations, creating difficulties when treating patients or performing vaccine research. After transmittance via the sandfly bite, the parasite is able to infect macrophages and avoid the immune response necessary for killing and clearance. I am currently working on identifying contributing factors to disease within the human model, analyzing human and parasite gene expression using high throughput sequencing. Our findings could lead to improved therapeutics and better vaccine research, both of which are respectively lacking and non-existent for this neglected tropical disease. Understanding this disease also helps in understanding the inner workings of the immune system, knowledge that is applicable in autoimmune disease, cancers, and pathogenic research.

Qian Yu (MOCB, Song Lab)

My research studies the host response to Neisseria gonorrhoeae, the bacterium causing gonorrhea, with a focus on female infection, because it can lead to severe complications. In females the major infection site is cervical epithelium, which has distinct properties at different anatomical regions, and these differences potentially influence host responses to pathogen. I have developed a novel ex vivo infection model and shown that gonococcal infection in this model closely mimics the infection in vivo. Using this model, I aim to examine the response of epithelial cells at different anatomical regions to gonococcal infection at cellular and molecular levels. Furthermore, using this infection model, I will identify the host cellular components that are utilized by the bacterium for infection in vivo. These host components have potential to be developed as treatment targets of gonorrhea as alternatives to the currently failing antibiotics.


2014-15 Vasudevan Achuthan
(BISI-MOCB, Jeff DeStefano Lab)

Vasu's research focuses on studying the impact of several small molecules on the behavior of HIV Reverse Transcriptase (RT). Investigating how the different small molecules affect the behavior of the enzyme and the efficiency of RT inhibitors will ultimately help in designing novel
inhibitors against the viral polymerase.

Achuthan V, Keith BJ, Connolly BA, DeStefano JJ., 2014, Human immunodeficiency virus reverse transcriptase displays dramatically higher fidelity under physiological magnesium conditions in vitro, J.Virol;88(15):8514-27

2012-2013 Chaohong Liu
(CBMG Graduate Program, Graduated Sp2013, Wenxia Song Lab)

Current position: Post doc researcher at St. Jude's Children's Hospital

Chaohong's research on the molecular mechanism by which the actin cytoskeleton regulates the activation of B cell receptor (BCR) and B cells in response to antigenic signals. In a physiological situation, those antigenic signals are usually proteins or polysaccharides that could from the infectious agents. Such as the coats, capsules, cell walls, flagella, and toxins from bacteria, viruses, and other microorganisms. Lipids and nucleic acids are antigenic only when combined with proteins and polysaccharides. In our research, we used antibody specific for the BCR to mimic the protein antigens.

First Author Publications

  • Liu, C., H. Miller, G. Orlowsky, S. Sharma, H-K Lam, B. Grooman, S. Bolland, A. Upadhyaya, and W. Song. 2011. A balance between Btk and SHIP-1 activation regulate B cell receptor clustering via modulating actin remodeling. J. Immunol. 187(1):230-9.
  • Liu, C., X. Bai, J. Wu, S. Sharma, A. Upadhyaya, C. I. M. Dahlberg, L. S. Westerberg, S. B. Snapper, X. Zhao, and W. Song#. 2013. N-WASP is essential for the negative regulation of B cell receptor signaling. PLOS Biol. 11(11): e1001704.
  • Liu, C., M. K. Fallen, H. Miller, A. Upadhyaya, and  Song, W#. 2013. The actin cytoskeleton coordinates the signal transduction and antigen processing functions of the B cell antigen receptor. Front. Biol. 8(5):475-485.
  •  Liu, C., H. Miller, S. Sharma, A. Beaven, A. Upadhyaya, and W. Song#. 2012. Analyzing actin dynamics during the activation of the B cell receptor in live B cells. Biochem. Biophys. Res. Commun. 427(1):202-6
  • Liu, C., H. Miller, G. Orlowski, H. Hang, A. Upadhyaya, and W. Song#. 2012. Actin reorganization is required for the formation of polarized BCR signalosomes in response to both soluble and membrane-associated antigens. J. Immunol. 188(7):3237-46.
  • Liu, C., H. Miller, G. Orlowsky, S. Sharma, H-K Lam, B. Grooman, S. Bolland, A. Upadhyaya, and W. Song#. 2011. A balance between Btk and SHIP-1 activation regulate B cell receptor clustering via modulating actin remodeling. J. Immunol. 187(1):230-9