Department: Scholars

Hi, my name is DeJuana Ford. I grew up in Newnan, Georgia and went to college at the University of Georgia in Athens, where I graduated with a degree in Genetics.

I have been passionate about science for as long as I can remember, but I became interested in the field of human genetics in particular after my 9^th grade biology teacher gave a lecture on how scientists use genetic markers to track human migration patterns.

For over ten years, my mother has battled systemic Scleroderma, which is an autoimmune disorder. I’ve been actively involved in an organization that provides support to Scleroderma patients. Watching my mother and other patients struggle to overcome the daily obstacles associated with incurable chronic illness inspired me to use my passion for science to explore questions that might improve people’s lives. Working in Dr. Melissa Davis’ lab as an undergraduate further cultivated my passion for the process of research and led me to seek a career in academic research.I am most interested in the field of human genetics, especially as it relates to the study of autoimmune disease, immunology, and cancer immunology.

Ultimately, I aim to have a career that incorporates academic research, teaching, and community outreach. As a researcher, my goal is to gain a better understanding of the genetic and environmental factors which drive the development of autoimmune diseases.

I joined the PREP program, because I was seeking opportunities to gain additional laboratory and research experience and to further enhance my communication skills. These experiences will prepare me to maximize my graduate education and ultimately to be a highly effective independent researcher.

PREP@UGA’s focus on infectious diseases has been especially beneficial for me, as I have a variety of opportunities to explore my interest in immunology.

I look forward to gaining excellent mentorship, learning new laboratory techniques, and building upon my scientific knowledge over the course of this year as a PREP@UGA scholar.

My faculty mentor is Dr. Melissa Davis in the Department of Genetics.

For the past decade, Dr. Davis has worked to gain a better understanding of the molecular and environmental factors driving tumor aggressiveness and breast cancer survival disparities. My project is focused on understanding the role that insulin-like growth factor pathway genes play in triple-negative breast cancer, which is a breast cancer subtype characterized by aggressive tumors that are unresponsive to hormone-based targeted therapies. Insulin-like growth factors, or IGFs are structurally similar to insulin, but are distinct in that they associate with a set of binding proteins that regulate their activity.

Recent studies have linked breast tumor aggressiveness with increased levels of IGF-II protein expression. Prior to becoming a PREP scholar, I along with other members of the Davis lab, observed that IGFBP6, IGF-II’s preferred binding partner demonstrates distinct patterns of expression and subcellular localization in triple negative breast cells.

Specifically, we noticed that in triple-negative cells, IGFBP6 tends to form aggregates at the edge of the nucleus and co-localize with IGF-II. This is significant, because exclusion of these aggregates from the nucleus could limit IGFBP6’s IGF-II-independent, pro-apoptotic activities within the nucleus. Also, IGF-II’s association with IGFBP6 might be prolonging the half-life of IGF-II, thus promoting cancer cell growth.

To further investigate this pattern, I used RNA interference to reduce IGFBP6 mRNA expression in cells derived from triple-negative tumors. To accomplish this, I extracted RNA from triple-negative breast cells and used cDNA synthesis, PCR, and finally, a transcription reaction to synthesize a double-stranded RNA fragment specific to IGFBP6. After transfecting triple-negative cells with the double-stranded RNA, I observed IGF-II expression and subcellular localization in these cells.

I hypothesized that IGF-II would be more evenly distributed throughout the cytoplasm after the IGFBP6 knockdown, and my preliminary data seem to support this hypothesis. This is significant, because it suggests that distinct IGFBP6 expression patterns have the potential to impact IGF-IIs cancer cell growth-promoting activities.

My next set of experiments will use qPCR to access whether the IGFBP6 knockdown in these cells impacted the expression of two anti-apoptotic, downstream targets of IGF-II. Taken together, these data will give us a better understanding of the molecular mechanisms by which the insulin-like growth factor pathway might impact triple-negative breast cancer.

My name is DeJuana Ford, and I am a PREP@UGA scholar.

Hi, my name is Ivelisse Resto. I grew up in Las Piedras, Puerto Rico and went to college at University of Puerto Rico, in Humacao, Puerto Rico and graduated with a Bachelor of Science in Microbiology.

I’ve always have a desire for knowledge and understanding of the unfamiliar aspects of the world that surrounds me. As I grew up, and with the support of my teachers, I began to participate in science and math competitions, which further increased my curiosity and triggered my interest in science.

As an undergraduate student, I had the opportunity to conduct research in prokaryotic biology for the first time during a summer research program at the University of Georgia, in Athens. During that time I was able to use critical thinking to contribute to the understanding of host-pathogen interactions. This very enriching experience, in addition to faculty encouragement, was fundamental in my decision to pursue graduate studies in biomedical research.

The general areas of research that I’m most interested in are immunology and virology .

My long-term career goals are to earn a PhD degree related to one or both of those areas, and then proceed to post-doctoral studies. Once these goals are reached, the next step in my career is to conduct research at academia level as well as to teach and advise the future generations to prepare them to succeed in their chosen career path.

Joining a PREP program would be the first step on my way to reach my career goals. A PREP program would help me gain more research experience in a laboratory, improve my research skills, and at the same time it would give me a glimpse of the life of a graduate student.

By participating at UGA’s REU summer program I was able to see and experiment firsthand the excellent and diverse training in pathogen biology and host/pathogen interactions UGA can provide. Together, faculty members, student mentors, and PREP@UGA coordinators provide a supportive environment and the necessary tools to help you go in the right direction to fulfill your established goal.

The type of preparation received from PREP @ UGA will make me a competitive candidate for graduate school and it will help me further explore my areas of interest.

My research mentor is David Rose, and my faculty mentor is Dr. Kimberly Klonowski.

Seasonal influenza is an acute viral infection that can affect anybody in any age group, however, infants and the elderly are most susceptible to infection. Annual epidemics of influenza worldwide result in about 3 to 5 million cases of severe illness, and about 250,000 to 500,000 deaths in these high risk populations. Variants of influenza virus that circulate every year are the result of changes in the surface proteins hemagglutinin (HA or H) and neuraminidase (NA or N). These proteins are important for the attachment, and eventual release, of the virus from host cells. Cells of the adaptive immune system, including B and T cells, are required for viral clearance. However, early viral control is mediated by innate immune cells like macrophages, natural killer cells (NK cells), and dendritic cells. NK cells are granular cytotoxic lymphocytes that are activated through cytokines and cell surface receptors, most which are not virus-specific. However, NK cells in mice and humans both express an activating receptor specific for influenza HA called NKp46. The overall goal of our research is to determine whether differences in HA expression and strain specificity regulates NK cell activation and downstream immunity or pathology. Our hypothesis is that NKp46 is key determinant regulating NK cell function after influenza infection.

To test our hypothesis, we will produce a recombinant NKp46 by means of molecular techniques such as bacterial transformation, transfection, and protein isolation. Once we determine we have correctly expressed our protein, we will then use the recombinant NKp46 to probe the interaction between NK cells and a library of HA  proteins from different influenza strains, like H3, H5 and H7. Specifically, we will determine whether the addition of our recombinant NKp46 protein to these co-cultures blocks NK cell activation and killing. This is measured by NK cell expression of CD69 and CD107a by flow cytometry and killing of the HA expressing cells in cytotoxicity assays.

My name is Ivelisse Resto and I am a PREP@UGA scholar. 

Hi, my name is Brent Allman. I grew up in San Diego, California and attended the University of San Diego where I graduated with a Bachelor of Arts in Mathematics with a minor in Biology.

I have always been one to ask questions. Growing up I was fascinated with the natural world and I began to develop interests in biology, recognizing the plethora of unanswered questions for study.

During my freshman year I immediately began working in a lab. I found the research process both fun and rewarding. Continuing research in the same lab for four years solidified in me the idea that scientific research allows one to contribute to the world’s collective body of knowledge.

At the beginning of my undergraduate career, I quickly realized I had an affinity for mathematics. As my intellectual interests matured, I discovered that mathematics is used as a powerful tool to study biological systems. For this reason, I want to pursue graduate training in quantitative biology so I can master tools in computational biology and bioinformatics.

Once I obtain a PhD, I will pursue post-doctoral training in industry or academia to continue developing myself as a successful independent researcher. My ultimate career goal is to become a professor a university that will allow me to both develop coursework and mentor students through research so they may be prepared for an interdisciplinary career path.

I decided to join a PREP program because I did not have the opportunity to pursue interdisciplinary research in my fields of interest during my undergraduate career. Before pursuing quantitative biology at the graduate level, I wanted more concrete experience in the field.

PREP@UGA is affiliated with many faculty members that have developed strong interdisciplinary research environments, particularly in quantitative biology.

While at UGA, I will be spending the majority of my time doing research while taking graduate courses and actively participating in seminars and journal clubs. I plan to develop both my wet and dry lab skills so I can be equipped for a variety of laboratory environments in graduate school.

My primary faculty mentor is Dr. Jessica Kissinger, and my secondary faculty mentor is Dr. Juan Gutierrez.

My project focuses on the apicomplexan parasite Toxoplasma gondii. Until recently, Toxoplasma gondii was believed to exhibit an almost exclusively clonal population structure. However, Dr. Kissinger and her colleagues analyzed genomes of 62 T. gondii strains and they suggest that their population structure involves more sex across evolutionary time than previously thought.

I will be creating a mathematical model to quantify how sexual recombination has played a role in the population structure and evolutionary history of the parasite. To do this I will be using genomic data of the 62 Toxoplasma strains to determine regions of the genome that may provide insights to their evolutionary past.

My name is Brent Allman and I am a PREP@UGA scholar. 

Hi, my name is Michael Mills. I am a United States citizen originally from Ghana, West Africa. I went to college at The University of Georgia, in Athens, Georgia and graduated with a degree in the Pharmaceutical Sciences.”

My ultimate goal, as a freshman, was to earn a doctorate degree in Pharmacy. This changed my sophomore year when I started working at Synageva Biopharmaceuticals. Through the experiences I gained from working in a rapidly growing Pharmaceutical company, I realized my interest lay in the ever-changing field of scientific research. As a result, I changed my degree track to the Pharmaceutical Sciences where I learned about the various aspects of drug formulation and delivery. This whet my appetite for research, and though I have broad interests in varying research areas, my experience in my current PREP lab has helped me recognize my attraction to Microbiology as a fundamental science. After graduate school, I plan to continue gaining experience as a post-doc before venturing into academia.

The PREP program was perfect for me because my late career change to the pharmaceutical sciences led to two semesters of research experience as an undergraduate student. I felt, THAT experience was not enough to prepare me for graduate school. Now I plan to use my time at PREP@UGA to be adequately prepared to perform in the best Microbiology graduate programs in the nation.

My current research and faculty mentor is Dr. Vincent Starai.

Brugia Malayi, a nematode pathogenic to humans, causes a crippling disease known as filariasis in tropical locations. This nematode harbors endosymbiotic bacteria from the genus Wolbachia, and these bacteria are known to be required for the nematode to survive within a host. Therefore, understanding how these bacteria live inside the nematode may provide information towards the treatment of filariasis.

Wolbachia Wbm0076 is a gene which encodes for an excreted protein of the bacterium. This protein is hypothesized to be required for the association of Wolbachia with the nematode. Interestingly, bioinformatics tell us that Wbm0076 belongs to the WAS family of proteins, which are involved in remodeling the actin cytoskeleton in eukaryotic cells. Using the yeast platform as a simple eukaryotic cell, my project involves studying the hypothesized role of the Wolbachia effector protein Wbm0076 in eukaryotic actin rearrangements.

To help drive my discoveries regarding Wbm0076 activity in host cells, I’ll be using a variety of laboratory techniques including yeast DNA transformations, molecular biology, fluorescence microscopy, Western blotting, PCR, and gel electrophoresis. These studies hope to identify key ways that this fascinating endosymbiotic bacterium can survive within a pathogenic nematode.

My name is Michael Mills and I am a PREP@UGA scholar.

Hi my name is Jessica Elmore. I grew up in Columbus, Georgia and I went to college at Howard University in Washington, D.C where I graduated with a degree in Biology.

My fascination with science began in grade school. My middle school science teacher, Dr. Kelly, made science exciting by teaching us how people made scientific discoveries.

I decided on a career in biomedical research when I was an undergraduate at Howard University. My college Microbiology & Immunology classes piqued my interests in pathogenic organisms and the host immune responses that protect us against them. A combination of rewarding laboratory research experiences and faculty encouragement solidified this decision.

I’m most interested in studying host-pathogen interactions of highly infectious agents that lack effective treatments and pose significant health concerns.

Working as an independent investigator in a government setting would be an ideal venue to realize this dream.

I joined the PREP program to gain additional research experiences surrounded by like-minded individuals in a supportive environment where everyone wants you to succeed.

I hope to achieve acceptance into a competitive doctoral graduate program where I can further hone the skills needed to become an independent researcher.

Dr. Wendy Watford is my faculty mentor. Her lab focuses on the regulation of immune responses by cytokines. My research mentor, Nicole Acuff, is a 4th year graduate student who studies Th17 immunity.

My project aims to determine how the host Tpl2 kinase regulates the antimicrobial functions of neutrophils, which are important first responders during an infection. I will evaluate neutrophil recruitment, phagocytosis of microbes, cytokine secretion, and the generation of antimicrobial reactive oxygen species in response microbes.

To address this, I will use a varied approach consisting of chemotaxis, phagocytosis, microscopy and gene expression assays, among others. My hypothesis is that Tpl2 is an essential positive regulator of neutrophil functions that promotes host defense.

My name is Jessica Elmore and I am a PREP@UGA scholar.

Hi, my name is De’Ashia Lee and I grew up in Pineland, SC.  I attended Howard University in Washington, DC where I graduated with a Bachelor’s of Science Degree in Biology.

My father passed away from sarcoidosis when I was very young.  At the time, I didn’t know anything about sarcoidoisis. Through independent research I learned that the cause of sarcoidosis is unknown, but the current hypothesis is that in genetically susceptible individuals sarcoidosis is caused through alteration  to the immune response after exposure to an environmental, occupation or infectious agent. The research surrounding sarcoidoisis made me very interested in science, particularly disease susceptibility and infectious diseases.

In college I further explored my interests in science by participating in different research training programs. I decided to pursue a career in research because you are constantly challenged to balance creativity with critical thinking. Research is one of the few career paths where you able to make contributions to answer some of the problems that affect society at large.

The research areas I am most interested in are antibiotic resistance, innate immunity, and the molecular biology of viral diseases.

My long-term career goal is to be employed by a government institution where I can apply my research training to addressing public health issues, such as vaccine development, and antibiotic resistance.

The goal of PREP programs is to strengthen the research skills and academic competitiveness for students who are interested in pursuing a graduate degree. I decided to participate in a PREP program because I wanted to take advantage of any opportunity that would allow me to be a competitive applicant to graduate schools.

PREP@UGA is the best program for me because of the focus on infectious disease research. The environment at UGA for infectious diseases research is excellent and the faculty is extremely knowledgeable and enthusiastic about their work. The amount of collaborations among all the principle investigators was also very encouraging and indicated that teamwork is an important component of the program.

I hope that my training from PREP@UGA will allow me to present a confident, competitive, and competent applicant to graduate programs.

My research mentor is Dr. Mattie Pawlowic and my faculty mentor is Dr. Boris Striepen.

Toxoplasma gondii is a parasite that causes severe disease in humans. Children, pregnant women, and immunocompromised individuals such as HIV/AIDS patients are particularly vulnerable. Toxoplasma gondii can infect humans in many ways; one way in particular is through drinking water contaminated with oocysts shed in cat feces. The oocysts have a tough outer shell that makes them resistant to conventional water treatments. My hypothesis is that certain lipids are critical to the formation of the tough oocyst shell. I will test my hypothesis by disrupting genes that encode enzymes that make lipids. I will make mutants by genetic engineering and then I will test the biological consequences of these changes. Each experience has allowed me to identify and cultivate my specific

Toxoplasma gondii is a good model to study this question because I can culture the parasites and change its genome by transfection. Specifically, I will make use of the CRISPR/Cas9 system to target the loci of the genes. I have already constructed the targeting plasmids. My next step is to isolate the mutants by drug selection and test them in a mouse model. I will collaborate with Dr. Dubey at the USDA to study the impact of my mutants in the cat, which is the definitive host of Toxoplasma gondii.

My name is De’Ashia Lee and I am a PREP@UGA scholar!

Hi, my name is Trent Frisbie. I grew up in Redding California and went to California State University, Stanislaus in Turlock, California.  I graduated with a Bachelor’s of Science in Biology with a concentration in Genetics and a minor in Chemistry.

I’ve always had a passion for science. I truly enjoy learning about new and upcoming research that paves the way for biological discoveries and innovations.

Earning a PhD allows me to answer questions in the form of a research project. It provides a unique opportunity to take a project from start to finish. The creative aspect of research allows me to study something that nobody else in the world is researching.

I am interested in variety of research topics broadly associated with genetics, including molecular and medical genetics, developmental biology, cancer genetics and molecular diagnostics.

In terms of a career, I envision myself not only teaching science, but also doing cutting-edge biomedical research. Earning a Ph.D. in biomedical science would advance my education and skillset by adding to my skills, both critical and creative, in working with science on a daily basis. I see the doctoral degree as a challenge and an opportunity to make strides toward my career goals.

I decided to join the PREP program to gain high-level research experience along with a first-hand look at what life as a graduate student is like.

The support that I have received from everyone in the program has been unparalleled. All the resources provide a great opportunity for success. Both the faculty and student mentors are very involved and truly want me to succeed.

My Faculty mentor is Nancy Manley and my research mentor is John O’Neil.

a. My project describes the effects of bone morphogenetic protein (BMP) signaling in the development of the third pharyngeal pouch.
b. The third pharyngeal pouch is an endodermally derived primordium that consists of progenitor cells that differentiate into thymus or parathyroid cells.
c. Foxn1 is used as a marker for thymus specification whereas GCM2 is a marker for parathyroid specification.
d. BMP is expressed in ventral pouch while Sonic Hedge Hog (SHH) is expressed in dorsal pouch.

Hypothesis: We hypothesize that BMP is necessary for normal fate specification and patterning of the thymus. Ultimately, BMP promotes thymus fate and inhibits parathyroid fate.

a. I am testing this hypothesis using an inducible Gremlin strain of transgenic mice in a tissue specific Cre-Lox induction system.
b. Cre-Lox technology uses the enzyme Cre recombinase to recombine separated Lox P sites, which results in the expression of Gremlin.
c. In using these inducible gremlin mice, I am able to knock-down BMP expression inspecific tissues at various stages of embryonic development.
d. In early developmental stages I’m using Sox17Cre and Foxa2CreE to drive Cre expression in the endoderm. Wnt1Cre is used to drive Cre expression in neural crest cells.
e. At a later stage I will use Foxn1Cre to determine secondary roles of SMP in thymus development.
f. Throughout my project I will use techniques like immunohistochemistry, in-situ hybridization and fluorescence activated cell sorting to determine how BMP affects pouch development.

My name is Trent Frisbie and I am a PREP@UGA Scholar.

Hi, my name is Kiara Miller. I grew up in Jonesboro, Georgia, and went to college at Savannah State University in Savannah Georgia. I graduated with a Bachelor of Science in Biology

I first became interested in science by watching Bill Nye the Science Guy on television. There is an episode in which he explains that there is science in music because of the vibrations and travel of sound, and then there is a huge musical number. Following this, I kept myself actively involved in science by entering a number of science fairs in elementary and middle school.

Because I attended a small liberal arts college where scientific research was not in the forefront, I was my own guide when looking for research opportunities. During my freshman year, I sought out many summer research programs, and I was fortunate to take part in an 8 week summer program at Georgia State University following the end of my first year. The research was funded by the National Institutes on Drug Abuse. My research project included localizing a specific receptor gene in the stomatogastric ganglion of the spiny lobster. After spending time in a graduate level environment and taking ownership of an independent project that yielded fantastic results, I knew that a career in research is what I want.

My primary interests lie in neuroscience, more specifically neurobiology of disease and aging, as well as neuroendocrinology.

My long-term career goals include successfully matriculating through graduate school to later take a postdoc position. However, I am still undecided about whether or not I will go into academia or industry, but lifelong research is a major part of these plans.

I joined a PREP program because although I had research experience, I felt that I needed a more extensive training before heading into graduate studies. I think of PREP as a second chance to prepare for one of the largest milestones in my life and a career as a scientist.

PREP@UGA is the best program for me because not only do I have the opportunity to work on an independent project, the program also gives us many opportunities for interdepartmental interaction among graduate students including enrollment in a few of the graduate courses. PREP also guarantees that we have opportunities to travel and present our research data. The program is truly preparing me for the road ahead.

First, I hope to gain admission to the graduate program of my choice; after all, PREP is tailored to preparing us to become critical thinkers and well-rounded scientists. I also hope to expand my knowledge of infectious diseases. Finally, I plan to build relationships with both of my mentors and my fellow PREP colleagues that will extend beyond this year that we are spending together.

My research mentors are Tara Bracken, a PhD candidate and Dr. Demba Sarr, a research scientist. My faculty mentor is Dr. Julie Moore.

The trophoblast is a layer of multinucleated placental cells that facilitates the exchange of waste, gas and nutrients between the maternal and fetal systems. When a mother is infected with malaria, parasite-infected red blood cells come into contact with the trophoblast. It has been theorized that this interaction leads to an immunological response that includes the recruitment of maternal inflammatory cells to the maternal blood space. This immunological response coupled with the activation of blood clotting, or coagulation, are characteristic of the pathogenesis of placental malaria. We hypothesize that this pathogenic environment prompts the release of small membrane vesicles called microparticles from the trophoblast. We are interested in microparticles and their characteristics because they are known to be released when cells are activated. We also hypothesize that many cell types will release microparticles in response to stimulation with components of the malaria parasite. In this case, the detection of trophoblast-specific microparticles that present indicators for procoagulant activity in maternal blood could serve as a novel diagnostic marker for placental malaria.

For my project, I will employ cell culture and flow cytometry. I will culture a human placenta choriocarcinoma cell line called BeWo. These cells will be stimulated with a number of malarial components including hemozoin, which is a byproduct that is formed when parasites consume hemoglobin inside the red blood cell. Additionally, they will be stimulated with culture medium, uninfected and infected RBC. Supernatants will be collected, and a flow cytometric analysis will be performed to determine the presence of microparticles. We expect that these cells will release microparticles in response to the stimulation with components of the malaria parasite but not in response to the medium and uninfected RBC. We further expect that the microparticles will have malaria-induced procoagulant activity. Using this in vitro approach, I will work with my mentors to refine a novel flow cytometric technique that will be used for the detection of cell-specific microparticles. This is especially significant because after optimizing this technique, we will ultimately apply it to clinical samples from women naturally exposed to malaria.

My name is Kiara Miller, and I am a PREP@UGA scholar.

I’m Enrico Barrozo. I went to Augsburg College in Minneapolis, MN where I earned a Bachelor’s of Science degree in Biology.  I’ve always been interested in the human condition. My mom passed away in April of this year and she was chronically ill for nearly 10 years. I was going in and out of hospitals and always being around physicians, I was constantly asking questions to find out what was wrong with my mom. This drove me to be a Biology Major. At Augsburg College I worked with my undergraduate mentor Dr. Matthew Beckman where I learned that I have a passion for research. I find research rewarding and intellectually stimulating. I’m driven by the possibility of discovery and innovation in the daily life of a scientist. I find research rewarding and intellectually stimulating. I’m driven by the possibility of innovation and discovery in the daily life of a scientist. Before this year I would’ve said I’m interested in genetics. However, genetics is a broad field and is more of an approach. I’m interested in personalized medicine and in the future I want to use pharamacogenetics, which is using a person’s unique genetic code to design therapies and prevent disease. Long term goals are to get a PhD where I learn basic science and techniques that will be essential to my future as a scientist. Next, I’ll get post doctorate training and that will determine what I will do for the rest of my life. Eventually, I want to be doing cutting-edge research in my own lab researching medical development or pharmaceuticals.

At Augsburg College I was passionate about a lot of things. A captain of the football team, doing research when I wasn’t in classes, working 2-3 part-time jobs, and working towards getting my degree. Last spring I was awarded with the Student Leader of the Year award for my accomplishments at Augsburg. This meant a lot to me but after graduation I wanted to redefine myself and focus more on my research. Here, in PREP@UGA I’m living the life of a graduate student. I work 40+ hours in a lab, take graduate level courses, and I’m learning essential techniques that will help me to hit the ground running when I’m accepted into a PhD program.

This post-baccalaureate training in infectious disease research will provide evidence that I can be a successful graduate student. I’ve shown that I’m fully dedicated to research and becoming a scientist. My faculty mentor is Dr. Biao He and I work with Shannon Phan, a 4th-year graduate student. I’m studying respiratory syncytial virus. (RSV) infects everyone by the age of 2 and there is currently no licensed vaccine. Symptoms result from lower respiratory infection and virulence of RSV increases when infecting infants, the elderly, and immunosuppressed.  Specifically, my project is investigating the interaction between RSV phosphoprotein (P) and host kinases on the RSV life cycle. The RSV-P protein is a heavily phosphorylated protein that stabilizes the RSV polymerase complex.  It is hypothesized that P phosphorylation by host kinases is important for viral transcription and replication, but the precise role is unclear.  Our goal is to determine which serine and threonine residues in RSV P are critical for RSV replication. Our approach includes… Designing primers to create plasmids encoding RSV P with serine and threonine residues mutated to alanine.  This will prevent phosphorylation at those sites in the P protein.  We will use standard cloning techniques such as polymerase chain reaction (PCR), splicing by overlap (SOE), digestion, ligation, and transformation into an E. coli plasmid. Next, we will be… Sequencing the plasmids with the P gene inserted to make sure the correct mutations have been introduced into the gene. Then, we will be… Using these plasmids to perform a luciferase-reporter-based minigenome assay to measure activity of the RSV replication complex. This assay will help us determine if the mutations have an effect on the transcription and replication of RSV.

My name is Enrico Barrozo and I am a PREP@UGA scholar.