BBSP Faculty
Experimental Evolution of Viruses. We use both computational and experimental approaches to understand how viruses adapt to their host environment. Our research attempts to determine how genome complexity constrains adaptation, and how virus ecology and genetics interact to determine whether a virus will shift to utilizing new host. In addition, we are trying to develop a framework for predicting which virus genes will contribute to adaptation in particular ecological scenarios such as frequent co-infection of hosts by multiple virus strains. For more information, and for advice on applying to graduate school at UNC, check out my lab website www.unc.edu/~cburch/lab.
We use the premier model plant species, Arabidopsis thaliana, and real world plant pathogens like the bacteria Pseudomonas syringae and the oomycete Hyaloperonospora parasitica to understand the molecular nature of the plant immune system, the diversity of pathogen virulence systems, and the evolutionary mechanisms that influence plant-pathogen interactions. All of our study organisms are sequenced, making the tools of genomics accessible.
The Gordon lab is brand new to UNC, and studies stem cell and stem cell niche biology in the model organism C. elegans. The germ line stem cells make the gametes, which make the next generation of worms. These cells are therefore at the nexus of development, genetics, and evolution. We will be getting started with projects pertaining to evolutionary comparative gene expression in the stem cells and stem cell niche and niche development. The techniques we use include molecular biology, CRISPR/Cas9-mediated genome editing, worm genetics, and microscopy.
Our research interests broadly span population genetics, statistical inference, and evolutionary genomics. We are interested in how evolutionary processes like changes in population size, recombination, mutation, selection and factors such as genome architecture shape patterns of genomic variation. Work in the lab involves employing computational and theoretical approaches, statistical method development, or using an empirical approach to perform evolutionary inference and ask fundamental questions in population genetics.
The goal of my research is to identify, clone, and characterize the evolution of genes underlying natural adaptations in order to determine the types of genes involved, how many and what types of genetic changes occurred, and the evolutionary history of these changes. Specific areas of research include: 1) Genetic analyses of adaptations and interspecific differences in Drosophila, 2) Molecular evolution and population genetics of new genes and 3) Evolutionary analysis of QTL and genomic data.
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.
Despite recent success in reducing malaria transmission, the estimated annual numbers of malaria infections (~225 million) and deaths (~781,000) remain high. Despite this immense burden, our understanding of the genetic diversity of malaria and the factors that promote this diversity is limited. This diversity among plasmodial parasites has a critical impact on many factors involved in the control of infections, including: 1) development of drug resistance, 2) development of naturally acquired immunity, and 3) vaccine design. My laboratory’s primary interests are: 1) describing the genetic diversity of P. falciparum using molecular biological and next generation sequencing tools, and 2) using these data to understand the evolutionary and ecological factors that drive this diversity, promote the emergence of drug resistance and affect our ability to effectively develop immunity.
Traditionally, basic science has sought to enter the translational pipeline through what can be referred to as “Bottom-Up” science, that is, studies that start with a hypothesis in the lab and aim to develop clinical relevance of the findings. In some cases, notably in conventional antibiotic development, this has worked well – but it assumes one-size fits all solutions that are only as good as our assumptions about the biology of many infectious diseases such as tuberculosis. By contrast, my research focuses on a “Top-Down” approach, leveraging the power of bacterial population genomics to identify bacterial processes important for Mtb success in people and to then employ cutting-edge experimental techniques to mechanistically dissect these processes with the goal of leveraging them using new translational tools.
In my work to date, I have applied this “Top-Down” strategy to define bacterial determinants of treatment outcomes and transmission success, as evident in first-author/corresponding author publications in prestigious journals such as Science, Nature Ecology Evolution, Cell Host Microbe, Science Advances, Genome Biology, PNAS, etc. My work combines expertise in evolutionary biology and bacterial genomics, cutting-edge bacterial genetics and high-throughput experimental phenotyping.
In my own lab, I will use these tools to (1) define the biological mechanisms that enable Mtb to survive antibiotic treatment; (2) identify bacterial determinants of TB transmission success; and (3) elucidate the evolutionary mechanisms underlying the emergence of new bacterial pathogens.
My research program studies how species form. We use a combination of approaches that range from field biology, behavior, and computational biology.
My work focuses on the role of plant pathogens in (A) controlling or facilitating biological invasions by plants, (B) structuring plant communities, and (C) modulating the effects of global change on terrestrial ecosystems. My group works on viruses, bacteria, and fungi that infect wild plants, chiefly grasses and other herbaceous species. Ultimately, I am interested in the implications of these processes for the sustainable provisioning of ecosystem services and for the conservation of biological diversity.
Dr. Parr’s research focuses on the infectious diseases of poverty, with translational projects in the Democratic Republic of the Congo (DRC) and other sites. His research concentrates on the molecular epidemiology of malaria and the evolution of “diagnostic-resistant” strains of Plasmodium falciparum, in particular. As a founding member of a World Health Organization laboratory network, he collaborates with malaria control programs and ministries of health to support surveillance of these parasites across Africa. His recent work in Ethiopia uncovered genetic signatures of strong positive selection favoring parasites with pfhrp2 gene deletion and influenced malaria diagnostic and surveillance policy in the Horn of Africa.
Dr. Parr has recently expanded his research program to include studies of other diseases that disproportionately impact marginalized populations worldwide, including viral hepatitis and syphilis, and serves as the director of the genomics core for a large NIH-funded syphilis vaccine development project that spans sites in Malawi, Columbia, China, North Carolina, and the Czech Republic.
Rotating students can expect to undertake translational projects that apply cutting-edge methodologies to real-world problems. Examples include application of novel enrichment methods that enable pathogen genomic sequencing from challenging field samples, development of CRISPR-based diagnostic assays, and evaluation of how infectious disease interventions affect pathogen population structure. Trainees will interact with diverse investigators and benefit from a highly collegial training environment in the Infectious Disease Epidemiology and Ecology Lab.
Dr. Parr continues to attend on the infectious disease inpatient services at UNC Medical Center and, in response to the pandemic, co-directed the UNC division of infectious diseases’ inpatient COVID-19 services. He also serves as Associate Editor for global health for Healthcare: The Journal of Delivery Science and Innovation. Dr. Parr and his work have been featured in the New York Times, Washington Post, CNN, and other media outlets.
I am a surgeon-scientist specialized in head and neck cancers. My goal is to address translationalquestions with genomic data and bioinformatic methods, as well as benchtop experimentation. My clinical practice as a head and neck cancer surgeon also influences my research by helping me seek solutions to problems that will directly inform gaps in the current treatment protocols.
I have developed a strong interest in HPV genomics as well as HPV/host genome integrations, as these factors are intrinsically related to transcriptional diversity and patient outcomes in HPV-associated head and neck cancers. Our work has helped to demonstrate that a novel mechanism of HPV-mediated oncogenesis requiring NF-kB activation is present in nearly 50% of oropharyngeal tumors. In this vein, we are aggressively investigating the cellular interplay between the NF-kB pathway and persistent HPV infection, tumor radiation response, NRF2 signaling, and more.
Another outgrowth of this work has been investigating APOBEC3B and its non-canonical roles in regulating transcription. Our preliminary work has demonstrated that APOBEC3B has surprisingly strong transcriptional effects in HPV+ HNSCC cells and may promote oncogenesis and tumor maintenance by suppressing the innate immune response and influencing the HPV viral lifecycle.
Our group also have a strong interest in translational genomic studies. Our group is working to develop methods that will make gene expression-based biomarkers more successful in the clinic, as well as studying many aspects of genomic alterations that contribute to the development of squamous cell carcinomas.
The Schrider Lab develops and applies computational tools to use population genetic datasets to make inferences about evolutionary history. Our research areas include but are not limited to: characterizing the effects natural selection on genetic variation within species, identifying genes responsible for recent adaptation, detecting genomic copy number variants and other weird types of mutations, and adapting machine learning tools for application to questions in population genetics and evolution. Study organisms include humans, the fruit fly Drosophila melanogaster and its relatives, and the malaria vector mosquito Anopheles gambiae.
First, we study the complex HIV-1 population that exists within a person. We use this complexity to ask questions about viral evolution, transmission, compartmentalization, and pathogenesis. Second, we are exploring the impact of drug resistance on viral fitness and identifying new drug targets in the viral protein processing pathway. Third, we participate in a collaborative effort to develop an HIV-1 vaccine. Fourth, we are using mutagenesis to determine the role of RNA secondary structure in viral replication.
We are a quantitative genetics lab interested the relationship between genes and complex disease. Most of our work focuses on developing statistical and computational techniques for the design and analysis of genetic experiments in animal models. This includes, for example: Bayesian hierarchical modeling of gene by drug effects in crosses of inbred mouse strains; statistical methods for identifying quantitative trait loci (QTL) in a variety of experimental mouse populations (including the Collaborative Cross); computational methods for optimal design of studies on parent of origin effects; modeling of diet by gene by parentage interactions that affecting psychiatric disease; detection and estimation of genetic effects on phenotypic variability. For more information, visit the lab website.
Our lab uses computational and molecular tools to study the evolution of genome organization, primarily in the flowering plants. Areas of
investigation include the origin and consequences of differences in gene order within populations and between species, the evolutionary and functional diversification of gene families (phytome.org), and the application of genomics to evolutionary model organisms (mimulusevolution.org). We also are involved in a number of cyberinfrastructure initiatives through the National Evolutionary Synthesis Center (nescent.org), including work on digital scientific libraries (datadryad.org), open bioinformatic software development (e.g. gmod.org) and the application of semantic web technologies to biological data integration (phenoscape.org).
My lab concentrates on studying the molecular genetic basis of the evolutionary processes of adaptation and speciation. The questions we ask are what are the sequence changes that lead to variation between species and diversity within species, and what can these changes tell us about the processes that lead to their evolution. We use a number of different techniques to answer these questions, including molecular biology, sequence analyses (i.e. population genetics and molecular evolution techniques), physiological studies, and examinations of whole-organism fitness. Currently work in the lab has focused on a intertidal copepod species that is an excellent model for the initial stages of speciation (and also provides opportunities to study how populations of this species adapt to their physical environment).