Research Interest: Virology
| Name | PhD Program | Research Interest | Publications |
|---|---|---|
| Ferris, Marty WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
In the Ferris lab, we use genetically diverse mouse strains to better understand the role of genetic variation in immune responses to a variety of insults. We then study these variants mechanistically. We also develop genetic and genomic datasets and resources to better identify genetic features associated with these immunological differences. |
| Baxter, Tori WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
My research aims to understand the pathogenesis and host immune response to emerging and re-emerging viral infections, including encephalitic alphaviruses such as chikungunya virus and respiratory coronaviruses such as SARS-CoV-2. Other areas of interest include examination of genetic and environmental factors that influence the response to infection and disease outcome, evaluation of vaccines and novel therapeutics against emerging viruses, and development and optimization of animal models of infectious disease. |
| Rubinsteyn, Alex WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
I work on predicting the determinants of adaptive immune responses. Most of my work has focused on T-cell epitope prediction for mutant antigens derived from cancer. I have collaborated closely with clinical groups to translate this work in personalized cancer vaccine trials. More recently I have also been working on joint T-cell and B-cell prediction for viral pathogens. The technologies and techniques applied across all of my projects are at the intersection of computational immunology, genomics, and machine learning. |
| 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. |
| 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. |
| Jiang, Guochun WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Antiretroviral therapy (ART) is effective in suppressing HIV-1 replication in the periphery, however, it fails to eradicate HIV-1 reservoirs in patients. The main barrier for HIV cure is the latent HIV-1, hiding inside the immune cells where no or very low level of viral particles are made. This prevents our immune system to recognize the latent reservoirs to clear the infection. The main goal of my laboratory is to discover the molecular mechanisms how HIV-1 achieves its latent state and to translate our understanding of HIV latency into therapeutic intervention. Several research programs are undertaking in my lab with a focus of epigenetic regulation of HIV latency, including molecular mechanisms of HIV replication and latency establishment, host-virus interaction, innate immune response to viral infection, and the role of microbiome in the gut health. Extensive in vitro HIV latency models, ex vivo patient latency models, and in vivo patient and rhesus macaque models of AIDS are carried out in my lab. Multiple tools are applied in our studies, including RNA-seq, proteomics, metabolomics, highly sensitive digital droplet PCR and tissue RNA/DNAscope, digital ELISA, and modern and traditional molecular biological and biochemical techniques. We are also very interested in how non-CD4 expression cells in the Central Nervous System (CNS) get infected by HIV-1, how the unique interaction among HIV-1, immune cells, vascular cells, and neuron cells contributes to the initial seeding of latent reservoirs in the CNS, and whether we can target the unique viral infection and latency signaling pathways to attack HIV reservoirs in CNS for a cure/remission of HIV-1 and HIV-associated neurocognitive disorders (HAND). We have developed multiple tools to attack HIV latency, including latency reversal agents for “Shock and Kill” strategy, such as histone deacetylase inhibitors and ingenol family compounds of protein kinase C agonists, and latency enforcing agents for deep silencing of latent HIV-1. Several clinical and pre-clinical studies are being tested to evaluate their potential to eradicate latent HIV reservoirs in vivo. We are actively recruiting postdocs, visiting scholars, and technicians. Rotation graduate students and undergraduate students are welcome to join my lab, located in the UNC HIV Cure Center, for these exciting HIV cure research projects. |
| 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.” |
| Martinez, Jennifer WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The focus of the work in the Martinez lab is to examine the non-canonical roles for the autophagy machinery during inflammation. Our recent work about LC3-associated phagocytosis (LAP) higlights the importance of this non-canonical autophagic process in maintaining tolerance and preventing unwanted autoinflammatory pathologies. |
| Griffith, Jack WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
We are interested in basic DNA-protein interactions as related to – DNA replication, DNA repair and telomere function. We utilize a combination of state of the art molecular and biochemical methods together with high resolution electron microscopes. |