Sunday, May 01, 2016
Ten undergraduate students participated in the 2016 Undergraduate Microbiology Research poster session, they included Alyssa Conrad (poster winner), Erika Feutz, Ariel Kleinschmidt, Paige Kies, Junlan Ma, Kayla Ladd, Lincoln Lewerke, Vishal Perera, Carly Twigg, and Luisa Valente.
Read the following selected research descriptions from the participants.
Alyssa Conrad: She is the undergraduate department poster winner, congratulations, Alyssa!!
My poster title is: "Respiratory Syncytial Virus Strains Induce Differential Innate Immune and CD4 T Cell Responses". Respiratory syncytial virus (RSV) is the most frequent cause of lower respiratory tract infections in young children resulting in respiratory disease that ranges from mild to severe. Severe RSV-induced respiratory disease in both animal models and infected infants is associated with elevated levels of pro-inflammatory cytokines including the Th17-associated cytokine IL-17. We compared the early inflammatory response induced by RSV strains known to elicit differential CD4 T cell responses following infection. In contrast to infection with the commonly used A2 strain of RSV, infection with the RSV line 19 strain resulted in increased levels of IL-6 and the inflammasome-associated cytokine IL-1β. In vivo neutralization and blocking experiments demonstrated that both IL-6 and IL-1β were required to induce the Th17 response following RSV line 19 infection. Infection of human monocytes with a panel of RSV strains revealed RSV strain-specific induction of IL-1β production. Similar RSV strain-specific induction of IL-1β was observed following infection of primary human alveolar macrophages, one of the initial cell types exposed to RSV in the lung. Together our results demonstrate that RSV strains differentially activate and influence both innate and adaptive immunity, likely contributing to the differential RSV pathogenesis observed in humans.
Erika Feutz: My poster title is "Analysis of Herpesvirus Cell to Cell Spread Factors",
All humans are infected with at least one herpesvirus with effects ranging from mild cold sores to life threatening cancers. Because of this, it is important to find a safe and effective treatment for most herpesviruses. To propagate the infection while evading the immune system, the newly produced virions must spread to the next cell via the cellular junctions. This process, which is called cell to cell spread, involves coordination between cellular and viral factors. We, and others, have identified proteins, specifically HSV-1 encoded UL51, gE, and UL7, that when deleted, show a significant spread defect but small replication defect. This result suggests that they all function on the same pathway in cell to cell spread. Suggesting that they may function as a single unit, UL51, gE, and UL7 pull down together in a co-immunoprecipitation experiment. From these results, we hypothesize that UL51, gE and UL7 function on the same pathway in cell to cell spread. This hypothesis predicts that a virus deleted for two of these genes would show a spread defect that is no worse than the worst of the two single deletions. We tested this by constructing two double deletion viruses and assaying for viral production and spread defects. In a UL51/UL7 double deletion, this hypothesis holds true. In a UL51/gE double deletion, this hypothesis held true on HaCaT cells, but not Vero cells, suggesting cell type dependent activity. We have also observed accelerated cellular cytopathic effect in UL51 mutants. We hypothesize that UL51 delays cytopathic effect to promote more efficient cell to cell spread. If this hypothesis holds true, mutants that have a plaque size defect should also demonstrate accelerated cytopathic effect. We are currently assaying five mutants for their cytopathic effect behavior.
Paige Kies: The poster title is " Interspecies Interactions Between Myxococcus xanthus and Bacillus subtilis".
M. xanthus and B. subtilis are common soil bacteria, each of which produce a large number of specialized metabolites and sporulate under nutrient limiting conditions to guarantee survival. While both organisms affect the composition and dynamics of microbial communities in soil, only M. xanthus is known to be a predator. Secretion of specialized metabolites and lytic enzymes are required for predation by M. xanthuswhile regulation of motility enhances its efficiency for predation. The ancestral strain, NCIB3610, resists predation by producing a specialized metabolite, bacillaene. Moreover, prolonged predator-prey interactions between M. xanthus and B. subtilis were found to induce formation of a new type of B. subtilis community designated as megastructures. This project seeks to study the dynamics of the interspecies interactions within a predator-prey relationship, ultimately culminating in sporulation and biofilm formation for both the predator and the prey.
Lincoln Lewerke:
All organisms must respond to the environment around them to maintain vital functions. Bacteria accomplish this task by altering the genes they express. One method of altering gene expression is through Extra-Cytoplasmic Function (ECF) sigma factors. I am interested in the ECF sigma factor σV, which responds to lysozyme, an antimicrobial enzyme used by the immune system to degrade the peptidoglycan of the bacterial cell wall which is essential for bacterial viability. σV is held in an inactive state by the anti-sigma factor RsiV. σV is released when RsiV is cleaved in the presence of lysozyme. Our lab is interested in discovering the role of the lysozyme-RsiV interaction that causes the release of σV, as well as, what protects RsiV from degradation in the absence of lysozyme.
Luisa Costa Oliveira Valente: My poster title is "Regulation of staphylococcal enterotoxin A in a slow growing Staphylococcus aureus strain".
Staphylococcus aureus is a bacterium that can cause many diseases, including boils, pneumonia, toxic shock syndrome, and food poisoning. This microorganism produces a lot of virulence factors that enables it to cause disease. One of them is staphylococcal enterotoxin A (SEA), which is related to food poisoning. This disease is preventable by good hygiene practices while preparing food, especially creamy pastries and sandwich fillings. Some people get chronically infected with S. aureus, and it can be due to strains that take a longer time to grow than usual, such as FRI 722. Besides showing this slow growing behavior, this strain produces a very high amount of this toxin, SEA. Therefore, it is important to find out why this strain grows slower, why it is able to produce that much SEA, if these two characteristics are related, and if other strains show the same behavior. This work aims to shed a light on S. aureus infections by slow growing strains, especially chronic, to lead to better diagnosis, treatment, and prevention.