PhD Program: Microbiology & Immunology
| Name | PhD Program | Research Interest | Publications |
|---|---|---|
| Thurlow, Lance PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
By 2035, more than 500 million people worldwide will be diagnosed with diabetes. Individuals with diabetes are prone to frequent and invasive infections that commonly manifest as skin and soft tissue infections (SSTIs). Staphylococcus aureus is the most commonly isolated pathogen from diabetic SSTI. S. aureus is a problematic pathogen that is responsible for tens of thousands of invasive infections and deaths annually in the US. Most S. aureus infections manifest as skin and soft tissue infections (SSTIs) that are usually self-resolving. However, in patients with comorbidities, particularly diabetes, S. aureus SSTIs can disseminate resulting in systemic disease including osteomyelitis, endocarditis and sepsis. The goal of my research is to understand the complex interactions between bacterial pathogens and the host innate immune response with focus on S. aureus and invasive infections associated with diabetes. My research is roughly divided into two project areas in order to understand the contributions of the pathogen and the host response to invasive infections associated with diabetes. Project 1: Defining mechanisms of immune suppression in diabetic infections. Project 2: Determine the role of bacterial metabolism in virulence potential and pathogenesis. |
| Sheahan, Tim WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Dr. Sheahan is an expert virologist with a primary appointment in the Department of Epidemiology in the Gillings School of Global Public Health and a secondary appointment in Microbiology and Immunology in the School of Medicine. His research is focused on understanding emerging viral diseases and developing new means to stop them with a current focus on coronavirus and hepacivirus. |
| Lin, Jessica WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Dr. Lin is an infectious disease physician-scientist whose research lies at the interface of clinical and molecular studies on malaria. My current projects focus on 1) determinants of malaria transmission from human hosts to mosquitos and 2) the epidemiology and relapse patterns of Plasmodium ovale in East Africa. Work in my lab involves applying molecular tools (real-time PCR, amplicon deep sequencing, whole genome sequencing, and to a lesser extent antigen and antibody assays) to samples collected in clinical field studies to learn about malaria epidemiology, transmission, and pathogenesis. |
| Mock, Jason WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our research interests focus on investigating the reparative processes critical to the resolution of acute lung injury. Acute events such as pneumonia, inhalational injury, trauma, or sepsis often damage the lung, impeding its primary function, gas exchange. The clinical syndrome these events can lead to is termed Acute Respiratory Distress Syndrome (ARDS). ARDS is a common pulmonary disease often seen and treated in intensive care units. Despite decades of research into the pathogenesis underlying the development of ARDS, mortality remains high. Our laboratory has built upon exciting observations by our group and others on the importance of how the lung repairs after injury. One type of white blood cell, the Foxp3+ regulatory T cell (Treg), appears essential in resolving ARDS in experimental models of lung injury–through modulating immune responses and enhancing alveolar epithelial proliferation and tissue repair. Importantly, Tregs are present in patients with ARDS, and our lab has found that subsets of Tregs may play a role in recovery from ARDS. |
| Vogt, Matthew WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
We want to understand why common pediatric respiratory virus infections cause severe disease in some people. Currently we focus on enterovirus D68, which typically causes colds but rarely causes acute flaccid myelitis, a polio-like paralyzing illness in children. We study both the pathogen and the host immune response, as both can contribute to pathogenesis. Projects focus on use of reverse genetic systems to create reporter viruses to infect both human respiratory epithelial cultures and small animal models such as mice. Human monoclonal antibody effects on pathogenesis are also of interest. |
| Joseph, Sarah B. PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
We use studies of HIV/SIV evolution to reveal information about viral dynamics in vivo. This typically involves genetic and/or phenotypic analyses of viral populations in samples from HIV-infected humans or SIV-infected nonhuman primates (NHPs). We are currently exploring the mechanisms that contribute to neurocognitive impairment in HIV-infected people by sequencing viral populations in the CNS of humans and NHPs not on antiretroviral therapy. We are also using these approaches to examine viral populations that persist during long-term antiretroviral therapy in an effort to better understand the viral reservoirs that must be targeted in order to cure HIV-infected people. |
| Wallet, Shannon PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
My research interests are focused on mechanisms associated with altered innate immune functions, which lead to dysregulated adaptive immunity. Currently my research program has three major arms integrated through with a central philosophy. Specifically, our laboratory focuses on the contribution of epithelial cell biology and signaling to innate and adaptive immune homeostasis and dysfunction. We study the contribution of what I term ‘epithelial cell innate immune (dys)function’ to three major disease conditions: pancreatic cancer, type 1 diabetes (autoimmunity), and periodontal disease (autoinflammation). While appearing to be a diverse research program, we have found that many of the mechanisms and systems in play are surprisingly (or maybe not so surprisingly) similar allowing for rapid translation of our findings. Importantly, previous investigations into the role of epithelial cells in immunobiology have been hindered by a lack of robust primary cell culture techniques, which our laboratory has been able to overcome using both animal and human tissues. Thus, using our novel and unique tools we are able to evaluate our findings in the human conditions, again making translation of our findings that much more feasible. In addition to my primary research objectives, my collaborative research programs, have allowed me to be involved, at some level, in investigating the basic biology of health, multiple autoimmune conditions, autoinflammation, sepsis, and exercise induced inflammation I have been blessed with the opportunities to couple my passions and expertise with that of others to bring together multiple research communities with the goal of advancing human health and hope to be able to continue to do so for years to come. |
| Browne, Edward WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
We study the molecular mechanisms of HIV latency. Transcriptional silencing of HIV is a key mechanism of persistence in patients, and is a barrier to viral eradication, but little is known about the latent reservoir or the molecular mechanisms that regulate it. As such, our repertoire of drugs for targeting latently infected cells is limited. Some latency reversing agents (LRAs) have been developed, but these are typically reactivate only a minor subset of proviruses. This inefficiency is in part due to the reservoir not constituting a uniform target, but instead being a heterogeneous set of cells with diverse characteristics and restrictions to HIV expression. However, most analyses of latency use bulk cell cultures assays in which crucial information about the behavior of individual cells is lost. Also, latently infected cells in patient samples are exceedingly rare, making them very difficult to study directly. New technological breakthroughs in the field of single cell analysis as well as the development of primary cell models for HIV latency now open the possibility of observing how latently infected cells form and are maintained at single cell resolution. Our lab has developed tools to study the establishment, maintenance and reversal of HIV latency at single cell resolution using multi-omics methods. Furthermore, we combine these approaches with genetic perturbation, time-lapse microscopy and novel bioengineering tools to gain insight into how the host cell regulates HIV latency. We have recently discovered using single cell RNAseq (scRNAseq) that latency in primary CD4 T cells is associated with expression of a distinct transcriptional signature (Bradley et al 2018). Our hypothesis is that this signature represents part of a cellular program that regulates latency, and that this program is an exciting novel target for the development of LRAs. Ongoing projects in the lab involve the application of new technologies to our model systems, and testing/validation of the roles of host cell pathways we have identified in HIV latency. Our overall goal is to identify new targets for the development of drugs to clear the HIV reservoir. |
| Milner, Justin WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The overall focus of our lab is to develop new and exciting approaches for enhancing the efficacy of cancer immunotherapies. We utilize cutting-edge techniques to identify transcriptional and epigenetic regulators controlling T cell differentiation and function in the tumor microenvironment, and we seek to leverage this insight to reprogram or tailor the activity of T cells in cancer. Our group is also interested in understanding how to harness or manipulate T cell function to improve vaccines and immunotherapies for acute and chronic infections. |
| Cameron, Craig E. WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our laboratory now studies mechanisms of genome replication and pathogenesis of respiratory enteroviruses and evolution of neurovirulence using the tools of mechanistic enzymology, cell biology, stem-cell engineering, and virology. Our laboratory is also pioneering the development of tools to monitor viral infection dynamics on the single-cell level, aka “single-cell virology.” |