Center Events

Haley Aull - Graduate Student, Immunology, Microbiology, and Virology Ph.D. Program

BST2/Tetherin is an antiviral factor that broadly restricts enveloped viruses. BST2 tethers nascent virions to the cell surface by embedding itself into cellular and viral membranes. Tethering not only limits viral release, it also facilitates adaptive immune recognition of the infecting virus. Tethered virions are opsonized by antibodies, which can be recognized by Fc receptors on both natural killer cells and macrophages, activating said effector to phagocytose or kill the infected target cell.

Previously, we have identified that SARS-CoV-2 is susceptible to BST2 restriction. However, the virus has evolved to use its Spike to downregulate BST2. Downregulation is achieved by an interaction between Spike and the extracellular domains of BST2, routing BST2 for lysosomal degradation in a Clathrin- and Ubiquitin-dependent manner. Additionally, we found that later variants of concern have enhanced abilities to downregulate BST2, such that they completely escape BST2’s restriction. Here, we asked (1) the mechanism by which Spike routes BST2 for lysosomal degradation, and (2) what implications BST2 antagonism has on antibody-mediated cellular responses. First, I have identified that BST2 is ubiquitinated in the presence of Spike, and this ubiquitination is required for its downregulation. Next, I have identified that the clathrin adaptor AP1 is required for Spike mediated downregulation of BST2. Finally, to test whether BST2 antagonism relieves pressure from antibody-mediated cellular responses such as ADCC and ADCP, I have adapted reporter virus-based systems to measure infected cell killing and phagocytosis. Using this assay, I have demonstrated that BST2 enhances both ADCC and ADCP killing of SARS-CoV-2 infected cells.

 Dec 05, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Ruth Serra-Moreno, PhD

Jordana Schmierer - PhD Candidate, Immunology, Microbiology, and Virology Ph.D. Program

 Nov 19, 2024 @ 2:00 p.m.

 Medical Center | K207 (2-6408)

Host: Advisor: Toru Takimoto, PhD

David T. Evans, PhD - Professor, WNPRC Associate Director of Research Services Pathology and Lab Medicine
University of Wisconsin-Madison

We will review features of the HIV-1 envelope glycoprotein (Env) that confer resistance to antibodies and fundamental differences between neutralizing and non-neutralizing antibodies. New data will be presented on Fc-mediated antibody effector functions and adeno-associate virus (AAV) delivery of Env-specific antibodies to achieve durable, antiretroviral-free containment of simian immunodeficiency virus (SIV) infection in nonhuman primates.

 Nov 18, 2024 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Ruth Serra-Moreno, PhD

Shahad Ahmed - PhD Candidate, Immunology, Microbiology, and Virology Ph.D. Program

Serine incorporator 5 (SERINC5) is a cellular factor present in all eukaryotes and plays multiple roles in host defense. In 2015, SERINC5 was identified as a host restriction factor against retroviruses including HIV-1. SERINC5 proteins present at the membranes of virus-producing cells are incorporated into the budding retroviral particles and impair their ability to successfully infect new target cells. After this initial discovery, other groups demonstrated that SERINC5 similarly impairs the infectivity of influenza and SARS-CoV-2. Furthermore, recent studies revealed that SERINC5 restricts other enveloped viruses through additional mechanisms. First, SERINC5 impairs hepatitis B virus (HBV) particle secretion by interfering with the glycosylation of HBV proteins. Second, SERINC5 restricts classical swine fever virus (CSFV) replication by enhancing MDA5-mediated type I interferon signaling. Finally, we recently uncovered that SERINC5 also inhibits HIV-1 gene expression, and consequently impairs virion production. Our subsequent studies revealed that SERINC5 achieves this by downregulating HIV transcription, without affecting mRNA or protein stability. Consistent with these findings, we observed that SERINC5 similarly downregulates gene expression of plasmids and non-integrated proviral DNA. Our findings demonstrate that SERINC5’s actions in host defense extend beyond blocking HIV-1 entry and suggest that this restriction factor can also protect against multiple DNA pathogens that rely on cellular transcription machinery.

 Nov 13, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Ruth Serra-Moreno, PhD

Christian Melander, PhD - George & Winifred Clark Professor, Department of Chemistry & Biochemistry, University of Notre Dame

The rising incidence of multi-drug resistant bacterial infections coupled with the exit of antibiotic development by major pharmaceutical companies has necessitated the exploration of alternative approaches to combating these life-threatening infections. This seminar will present our recent efforts towards the development of adjuvants for the treatment of chronic carriage of Salmonella infections both in vitro and in vivo as well as our efforts towards overcoming resistance to polymyxins, which are generally viewed as the antibiotics of last resort for the treatment of gram-negative infections.

 Nov 11, 2024 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Paul Dunman, PhD

Karli Sutton - PhD Candidate, Immunology, Microbiology, and Virology Ph.D. Program

Platelets are predominantly associated with their role in thrombosis and wound healing, however in more recent years, they have been credited with immunomodulatory functions as well. For example, at steady state, platelets are involved in maintaining homeostatic conditions, but upon aberrant activation due to a vascular event, chronic inflammation, or infection, platelets can cause undesirable immune cell activation and phenotypic shifts. With this in mind, it is important to study the effects of platelet activation in chronic inflammatory conditions such as Human Immunodeficiency Virus 1 (HIV-1). Both the virus itself and long-term use of combined antiretroviral therapies (cART) can cause persistent inflammation, thus leading to increased levels of platelet activation.

Our lab has previously shown that HIV infection results in a significant increase in platelet activation. Platelet activation leads to expression and upregulation CD62P (P-selectin) which binds to PSGL-1 on monocytes, leading to formation of platelet monocyte complexes (PMCs). Our lab has shown that activated platelets push monocytes from a classical (CD14++CD16- ) phenotype to a pro-inflammatory, non-classical (CD14+CD16++) phenotype. Along with a shift in monocyte phenotype, we have also observed a decrease in efficacy of platelet:MoDC (monocyte derived dendritic cell) complexes to stimulate effective T cell responses. In addition to physically binding to other immune cells, platelets degranulate when activated, releasing immunomodulatory molecules and cytokines into the environment. This leads us to hypothesize that platelets modulate monocyte/MoDC phenotype and function via secretion of increased levels of immunoregulatory/immunosuppressive molecules in people living with HIV.

This study aims to explore what platelet-derived molecules lead to these observed deficiencies and also if anti-platelet therapy such as aspirin or clopidogrel can rescue the dysfunction. To conduct this study, I used both PBMCs and platelets from a cohort of age and sex matched individuals living with and without HIV (PLWH/PLWOH), as well as PBMCs from commercially obtained leukopaks. I then studied the effects of both platelets and platelet-derived molecules on monocytes, immature MoDCs (iDCs), and Mature MoDCs (mDCs) through the use of ELISAs, full spectrum flow cytometry, RT-qPCR, and antigen uptake assays. Our results indicate that platelet-derived TGFβ is upregulated in people living with HIV (PLWH). This directly polarizes monocytes and MoDCs towards a more immunosuppressive phenotype. Furthermore, we have found that MoDCs from PLWH secrete significantly higher levels of IL-10 compared to PLWOH. This would suggest that PLWH may have monocyte and MoDC dysfunction induced by both increased platelet activation and HIV status as a whole. Future work will include mechanistic and functional studies to further elucidate the impact of these two molecules on MoDC dysfunction in PLWH.

 Nov 07, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Meera Singh, PhD

Ryan A. Langlois, PhD - Professor, Department of Microbiology and Immunology, University of Minnesota

The global virome is incredibly diverse and emerging viruses threaten global health. The risk of virus spillover from one host into another is increasing due climate change. Currently it is difficult to determine which viruses among the many thousands have the potential to infect humans and drive novel pandemics. Viruses face many barriers when encountering a new species. They must use host factors to enter and replicate and evade the antiviral immune system. How viruses overcome these barriers could help to uncover new virus-host biology and help inform pandemic risk prediction. To address this, we have developed two novel model systems to evaluate cross-species infection potential. We use mice from the pet store as a virus reservoir and expose different rodent species. We also take an unbiased approach at an unprecedented sale and measure replication of a library of viruses in a “fibroblast zoo”, which represent the diversity of Mammalia

 Nov 04, 2024 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Andrew Varble, PhD

John Yin, PhD - Vilas Distinguished Achievement Professor, Wisconsin Institute for Discovery, Department of Chemical and Biological Engineering

Defective virus genomes (DVGs) are ubiquitous byproducts of normal virus growth. Despite their defects and failure to productively infect host cells, DVGs exhibit diverse functions: interfering with normal virus growth, activating host innate immune responses, and co-transmitting with normal virus particles. These functions can contribute to disease severity in human patients, but the precise mechanisms remain largely unknown. This talk will show how DVGs from bacteriophage T7, vesicular stomatitis virus, and SARS-CoV-2 interfere, co-evolve, and co-transmit with their parent viruses, shedding light on facets of their underlying mechanisms. Finally, we propose that unraveling the complexities of DVGs in natural infections could unlock design rules for new antiviral therapeutics and strategies that resist viral escape.

 Oct 28, 2024 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Yan Sun, PhD

Ajay Akhade, PhD - Senior Research Associate, Institute for Systems Biology, Seattle, WA

Abstract: While the effect of bacterial molecules on host innate immune activation is very well studied, the converse i.e. how innate immune host factors affect pathogen state and in turn modulate virulence is less appreciated. Caspase-1, a key effector molecule involved in inflammasome activation by bacterial ligands like flagellin has a well established role in controlling the growth of intracellular pathogens like Salmonella by triggering a form of cell death called pyroptosis. We recently observed that caspase-1 activation controls temporal and biphasic expression of flagellin during Salmonella infection. Towards furthering our understanding of global impact of caspase-1 on Salmonella physiology, we used Pathogen-sequencing, a method for sensitive transcriptome profiling of intracellular bacteria to find that caspase-1 decreases the resistance of Salmonella to endogenous cationic antimicrobial peptides, and to Polymyxin B - a last resort drug against Gram-negative bacterial infections. Intriguingly, independent of its enzymatic activity and the inflammasome, caspase-1 repressed the activation of the resistance determining two-component signal transduction system, PhoPQ in intracellular Salmonella, thus demonstrating a non-canonical role for caspase-1 in host defense. Our findings take host caspase-1 beyond the well-studied inflammasomes and tie it to signal transduction and drug resistance of an intracellular pathogen. As an independent investigator, using multi-omics approach to understand the molecular basis of the spectrum of host innate immunity dependent alterations in the physiology of intracellular pathogens will be central to my research. This will not only help explore novel fundamental aspects of pathogen physiology but also dissect the interplay of innate immune factors and reveal candidates for host-directed therapeutic interventions in bacterial infections. I look forward to interacting with the strong research community of experts in microbial pathogenesis and host defense and exploring the wealth of resources at URMC.

Passcode: 495968

 Oct 24, 2024 @ 2:00 p.m.

 Medical Center | K307 (3-6408)

Charkira Patrick - PhD Candidate, IMV PhD Program

Autoimmune thyroid diseases, including Graves’ disease, affect up to 5% of the global population. For reasons that remain unclear, around 25% of these patients can develop thyroid eye disease (TED), a debilitating condition that can lead to ocular irritation, bulging eyes (proptosis), optic neuropathy and vision loss. In TED, the connective tissue behind the eye becomes inflamed, enlarged, and remodeled. TED has long perplexed scientists and additional studies are needed to better understand the complex pathophysiology of the disease. Risk factors for TED include: age, microvascular disease, and tobacco use. While many cells infiltrate the orbit during disease progression, resident orbital fibroblasts (OFs) drive pathology as they proliferate excessively and produce aberrant amounts of extracellular matrix (ECM) and inflammatory cytokines. Recent studies revealed that orbital tissues from TED patients contain high levels of platelet-derived growth factors (PDGF) and increased interleukin-13 (IL13) signaling. OFs express PDGF receptors (PDGFRs) and IL13 receptors and thus are poised to respond to these extracellular signals. OFs also express the aryl hydrocarbon receptor (AHR), a ligand activated transcription factor. The AHR responds to environmental toxins including components of cigarette smoke and dioxin, however, AHR also binds to short-lived, endogenously produced tryptophan derivatives. Activation of the AHR by these short-lived ligands blocks fibroblast growth and activation. We hypothesize that targeting the AHR mitigates PDGF and IL13 signaling thereby alleviating TED pathology. To test this hypothesis, I have cultured OFs isolated from TED patients and treated them with PDGF or IL13 in the presence or absence of the AHR ligands, 6-formylindo (3,2-b) carbazole (FICZ) and the bacterially derived molecule, tapinarof (recently approved for plaque psoriasis). After treatment, cells were collected and analyzed by Western blotting and qPCR for proliferation markers, signaling proteins and AHR target genes. Cell morphology and migration were also assayed. Activation of OFs with PDGF led to a robust increase in AKT phosphorylation and expression of thymidylate synthase, an enzyme involved in DNA precursor synthesis and cell proliferation. PDGF signaling also increased proliferation and cell migration. Activation of OFs with IL13 led to induction of ERK phosphorylation and expression of periostin, lysyl oxidase, and eotaxin. Activation of the AHR by FICZ and tapinarof blocked PDGF and IL13 signaling. These data suggest that activating the AHR with tapinarof may represent a novel therapeutic approach for TED.

 Oct 24, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisors: Collynn Woeller, PhD & Jacques Robert, PhD

Emily Britt - Graduate Student

Staphylococcus aureus is a prevalent human pathogen responsible for an array of invasive infections. One of the most common manifestations of S. aureus infection is osteomyelitis, or bone infection, including severe post-operative prosthetic joint infection (PJIs). Osteomyelitis infections are exacerbated in patients with co-morbidities including obesity and type 2 diabetes due to impaired immune function, which leads to chronic inflammation and poor healing. Immune dysfunction can be attributed to gut microbiome dysbiosis, characterized by altered community composition and abundance, with aberrant production of gut-immune axis metabolites. Our lab has previously determined that impact of gut dysbiosis and immune dysfunction on S. aureus osteomyelitis in a murine cohort and found that restoration of gut homeostasis in obese-type 2 diabetic (obese-T2D) mice via dietary fiber oligofructose feeding improved infection outcomes including lower S. aureus burden, less tissue damage, and decreased hyperinflammation. Furthermore, with dietary oligofructose feeding, we found an increased level of gut-microbial derived polyamine metabolites. Polyamines regulate a variety of cellular functions related to growth but are also characterized as immunoregulatory due to their role in altering gene expression profiles and differentiation states. Oral administration of spermine and spermidine to obese-T2D mice resulted in reduced infection severity to similar levels seen in OF supplemented mice, suggesting polyamines partially mediate the beneficial effects on osteomyelitis severity. Our goal is to understand how polyamines modulate immune - S. aureus interactions in an obese-T2D environment. I will use our oligofructose supplemented murine PJI model as well as various in vitro methods to investigate our questions. Today I will share my progress toward understanding how the healthy vs obese-T2D environment impact macrophage function in vitro and how polyamines may restore function. Then, I will discuss our findings on how the obese-T2D associated hyperglycemia and hyperfibrinogenemia impacts S. aureus clotting and in vitro abscess formation. Finally, I will discuss preliminary results from our host-S. aureus dual RNA sequencing experiment using hybrid capture to assess the transcriptional landscapes of both the host and S. aureus at the sight of infection. Collectively, my investigations will elucidate the impact of an obese-T2D environment on S. aureus osteomyelitis and define oligofructose and polyamine impacts on infection outcomes. This work has broad implications for how dietary prebiotics and microbiota metabolites can improve the immune response in immune challenged hosts.

 Oct 17, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Steve Gill, PhD

Nicholas Pokorzynski, PhD - Postdoctoral Research Associate, Department of Microbial Pathogenesis, Yale University School of Medicine

Abstract: Glucose is the preferred carbon source of most microorganisms. Why, then, does glucose lose its preferred status when the intracellular pathogen Salmonella enterica serovar Typhimurium is inside mammalian macrophages? We now establish that this surprising behavior results from macrophages provoking cytoplasmic Mg2+ starvation in S. Typhimurirum. Cytoplasmic Mg2+ starvation drastically reduces synthesis of cyclic adenosine monophosphate (cAMP), the allosteric activator of the cAMP receptor protein (CRP), master regulator of carbon utilization. The resulting reduction in cAMP concentration decreases transcription of CRP-cAMP-activated carbon utilization determinants, which reduces uptake of corresponding carbon sources and modifies metabolism. Rendering CRP activity cAMP independent or supplementation with exogenous cAMP overcomes transcriptional, transport, and metabolic restrictions caused by cytoplasmic Mg2+ starvation. S. Typhimurium’s reduced glucose preference inside macrophages reflects that transcription of the glucose uptake gene is far more sensitive to the amount of active CRP protein than transcription of other carbon uptake genes. By reducing CRP-cAMP activity, the intramacrophage environment restricts S. Typhimurium metabolism, consistent with decreased protein synthesis that slows pathogen growth, heightening tolerance to antimicrobial agents.

Zoom: https://urmc.zoom.us/j/94337654366?pwd=pezThiio47PqoHmC4aTy5bflDnEovb.1

Passcode: 051922

 Oct 14, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Maggie Lesch - PhD Candidate, Immunology, Microbiology, and Virology Ph.D. Program

Colorectal cancer (CRC) is a devastating malignancy that ranks as the second leading cause of cancer-related deaths, and fourth in cancer diagnoses annually in the United States. Among CRC cases, rectal cancer (RC) comprises one-third of cases, with over 50,000 people in the US diagnosed each year. Surgical resection is a treatment option for RC, however it can greatly reduce patients’ quality of life and unfortunately, some patients still experience recurrence. Recently, treatment paradigms have shifted towards organ preservation in RC through the adoption of the watch-and-wait approach in which patients undergo total neoadjuvant treatment with active surveillance, often avoiding surgery. While approximately 30% of patients experience a complete clinical response with this approach, most have an incomplete response to neoadjuvant therapy and ultimately require surgery or further therapy. Why this binary divide occurs is poorly understood, and there are no biomarkers for predicting response. To study this question, our lab has developed a clinically relevant orthotopic murine model of RC, in which administration of Short Course Radiation Therapy (SCRT) results in recapitulation of this binary responder/nonresponder phenotype seen in patients. Our model enables the study of both phenotypes during and following treatment. Using this model, we performed a series of experiments to investigate the molecular mechanisms driving this responder/nonresponder dichotomy. Specifically, RNA-sequencing of intratumoral cell populations, following SCRT, revealed an upregulation of the Type I Interferon (IFN) signaling pathway in responder tumors when compared to nonresponders. Type I IFNs have emerged as essential cytokines that mediate the antitumor immune response. Preliminary data has confirmed that responder tumors had higher concentrations of intratumoral Type I IFN protein that were maintained throughout treatment. Blockade of the Type I IFN receptors completely abrogated the responder phenotype further emphasizing the importance of these factors in dictating the responder/nonresponder divide. To explore what may mediate this effect, we investigated the influence of the microbiome, as pathogen associated molecular patterns (PAMPs) from radio-sensitive bacteria are known to contribute to Type I IFN production. To test this, we depleted the microbiota by administering antibiotics throughout SCRT treatment. This resulted in a decrease in responder tumors, indicating that the microbiome plays a significant role in mediating the therapeutic effect. Future experiments using fecal transplants and 16s sequencing will explore whether specific bacteria or subsets of bacteria govern the treatment response. These studies are clinically translatable and may identify noninvasive predictive biomarkers, with the potential to improve the efficacy of SCRT and increase the number of patients who respond to treatment.

 Oct 10, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Scott Gerber, PhD

Kumari “Kavita” Thakur, PhD - Associate Research Scientist, Division of Molecular, Cellular and Development Biology, Yale University

Abstract: Bacteria are equipped with intricate mechanisms to adapt to environmental stresses, many of which involve non-coding RNAs such as small RNAs (sRNAs) and riboswitches. These regulatory RNAs play pivotal roles in bacterial virulence, biofilm formation, and antibiotic resistance. My research focuses on unraveling the post-transcriptional regulation of gene expression in bacteria, especially through noncoding RNA-based mechanisms. I will discuss my recent work on the role of sRNAs and RNA-binding proteins, such as Hfq, in regulating bacterial responses to stress. I will highlight my discoveries on the role of intrinsically disordered domains in Hfq, a previously debated topic in the literature, which are crucial for RNA interactions and gene regulation. Additionally, I will present the discovery of a novel riboswitch that detects 8-oxoG, a product of bacterial DNA damage caused by oxidative stress, leading to gene regulation. These findings were investigated using a variety of in vivo and in vitro techniques, including genetic reporter fusions assays, RNA sequencing (RNA-seq), northern blotting, and in-line probing assays. Join us to explore the critical role of non-coding RNAs (sRNAs and riboswitches) in the regulation of gene expression and their impact in the coding world of bacteria.

Zoom: https://urmc.zoom.us/j/99319220852?pwd=IIXdtQikGkNO905Rm1flLoXnjZISK4.1

Passcode: 717782

 Oct 10, 2024 @ 10:00 a.m.

 Medical Center | K307 (3-6408)

Robert J. Binder, PhD - Professor, Department of Immunology, University of Pittsburgh

During cancer immunosurveillance, dendritic cells (DCs) play a central role in orchestrating T cell responses against emerging tumors. Capture of miniscule amounts of antigen along with tumor-derived costimulatory signals can drive maturation and activation of DCs. We have shown that expression of the heat shock protein receptor CD91 on DCs is essential in the cross-priming of T cell responses in the context of nascent tumors. In this presentation, the mechanisms of the HSP-CD91 pathway will be laid out in mouse and human disease, as well as novel approaches to cancer immunotherapy borne out of our findings.

 Oct 07, 2024 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Jacques Robert, PhD

Dr. Sang Lee, PhD - Faculty Candidate

 Oct 04, 2024 @ 12:30 p.m.

 Kornberg Medical Research Building | 3.9654

Host: Tim Mosmann, PhD

Taylor Jones - Graduate Student

Influenza is a respiratory virus that infects the airways and lungs. Viral replication in the lower respiratory tract can result in pneumonia and severe disease. Immunological memory established by prior infection, such as T cells resident in the tissue, or vaccination significantly reduces virus-related morbidity and mortality. Although tissue-resident memory CD8 T cells (TRM) can rapidly mobilize upon reinfection to prevent disease severity, vaccine platforms often overlook cellular responses. We aim to uncover how TRM develop and understand what regulates their retention. TRM are a memory T cell subset that remain in the tissues and do not recirculate. Human and mouse TRM can express the integrins CD49a/CD29 and CD103/B7, which bind to local lung ligands and can be induced by TGFb and IL-12.

CD49a is indispensable for TRM retention; however, less is known about where and when CD49a becomes necessary during the T-cell response. We have shown that by day 8 in the lungs, CD49a- populations decreased, while the CD49a+ continued to increase. Because CD49a function may be important during the acute phase, we first wanted to understand where and when TRM precursors are formed. We measured CD49a and CD103 expression in WT mice in the priming lymph node (mediastinal lymph node: mLN) between 4-6 days post influenza A infection. This revealed that CD49a and CD103 are detected as early as 5 DPI, indicating that signals in the mLN promote TRM integrin expression. We addressed whether the activated T cells in the mLN were destined to traffic to the lungs. Blocking mLN egress with FTY720 reduced flu-specific CD49a+ populations in the lungs. This indicated that the mLN is a source of flu-specific integrin-positive cells in the lungs.

Given that CD49a-expressing cells are primed during early infection, we determined if CD49a is required for lung retention during the memory phase. We developed a tamoxifen-inducible knockout model (iKO) to target CD49a specifically in CD8 T Cells. With this model, we found that CD49a gene deletion reduced frequencies of CD49a expression in iKO mice; however, these CD49a- cells were still detectable in the lungs 6 days after inducing gene deletion. From these experiments, we hypothesize that CD49a expression is induced during the acute phase and supports retention before the memory phase. Understanding how TRM are formed and retained can inform vaccine design and help produce sustained tissue-resident and cross-protective T cells.

 Oct 03, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: David Topham, PhD

Aoshu Zhong, PhD - Postdoctoral Fellow, Division of Molecular and Cellular Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Bethesda, MD

Abstract: Research into bacterial immunity has led to the discovery of critical tools for molecular biology, including restriction enzymes and CRISPR systems. In this seminar, I will discuss the characterization of a novel family of antiphage defense proteins in bacteria and archaea whose toxic activities are blocked by antitoxin proteins encoded within the same genes. Specifically, I discovered that the broadly distributed recombination-promoting nuclease (rpn) genes uniquely encode two proteins. The Rpn long proteins are toxic, while the variable C-terminal domains, which are translated separately, function as the antitoxin. Moreover, I found that the C-termini of the Rpn proteins contain unique four amino acid repeats whose number can vary widely across strains of the same species. I solved the first crystal structure of an Rpn family protein. Finally, I demonstrated Rpn proteins provide resistance to phages. I propose that many more intragenic-encoded proteins that serve regulatory roles remain to be discovered in all organisms.

Zoom Passcode: 087445

 Sep 30, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Molly Niska - Graduate Student

Generating an antigen-specific memory B cell (MBC) pool upon antigenic exposure is an essential component of the adaptive immune response. A proportion of MBCs generated in responding lymph nodes during an immune response enter the circulation and disperse to lymphoid tissues throughout the body. Due to its size and cellularity, the spleen has long been recognized as a reservoir of MBCs, but recent studies implicate a novel functional role. Recent analysis of the B cell receptor (BCR) repertoire through phylogenetic reconstruction revealed distinctive patterns of BCR clonality in circulating MBCs compared to spleen-resident MBCs. While all circulating MBCs had clonally related precursors in the spleen, the splenic MBC reservoir contained unique clones absent in the circulation. Based on this finding, the idea that the spleen “archives” MBC clones generated in past responses was proposed. Expanding this idea, we suggest that the spleen is a dynamic archive accumulating antigen-reactive MBCs reactive to past infections and maintaining clonal families across multiple MBC subsets. This is supported by recent studies describing phenotypically and functionally distinct splenic MBC subsets, such as a CD21hi MBC subset in the splenic marginal zone with enhanced responsiveness to activation and a spleen-resident population of self-renewing T-bethi MBCs.

Here, we interrogate hemagglutinin-reactive splenic MBC subsets and characterize their properties and contributions to anti-influenza immunity. We chose HA as a model antigen as this enables us to capture the dynamics of HA-specific MBC in the spleen, owing to the chronological circulation of influenza A strains in human populations. Furthermore, repeated exposure to HA adds another complexity to our analysis of the splenic MBC archive, as MBCs with certain HA reactivities may reveal unique phenotypic and functional features. Using an extensive flow cytometry panel consisting of both surface markers and HA probes, we identified the phenotypic subsets in which HA-reactive MBCs reside. Strikingly, most MBCs reactive to early-life HA probes were confined to the T-bet hi spleen resident, self-renewing population. Contrastingly, MBCs reactive to more recently circulating HAs were primarily found in the CD21hi compartment, poised for rapid response to re-exposure. The archive hypothesis was further reinforced upon evaluation of Ab reactivity, demonstrating retention of MBC reactivities across a broad range of HA vintages. Thus, we suggest the spleen is a dynamic archive, selectively preserving MBCs reactive to no longer circulating influenzas, while continuously accruing MBCs to circulating influenza A viruses. Moreover, the functional compartment where MBCs of different reactivities reside might reflect the breadth of HA reactivity and frequent or recent activation and expansion. By improving our understanding of MBC maintenance, we will be better suited to design and evaluate the effectiveness of vaccine candidates based on key biomarkers of durable, long-lasting immune memory.

 Sep 26, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisors: Martin Zand, MD, PhD and Tim Mosmann, PhD

Pu-Ting Dong, PhD - NIH/NIDCR K99 Postdoctoral Fellow, The ADA Forsyth Institute, Harvard University Cambridge, MA

Abstract: Optical imaging techniques, such as label-free chemical imaging and fluorescence in-situ hybridization (FISH), have emerged as indispensable tools for unraveling the complexity of polymicrobial communities. Label-free chemical imaging enables non-invasive, high-resolution visualization of molecular composition, providing insights into spatial and temporal metabolic activities without the need for exogenous markers. Complementing this, fluorescence in-situ hybridization facilitates the precise localization of specific nucleic acid sequences within cells, allowing for the targeted examination of genomic elements and microbial identification. My research will delve into the synergistic application of both label-free chemical imaging and next-generation multiplex FISH imaging, to offer a comprehensive perspective on the functional analyses of biological systems. The integration of these techniques will not only advance our understanding of cellular dynamics but also holds promise for diagnostic and therapeutic innovations in diverse biological research and clinical contexts.

Zoom Passcode: 396091

 Sep 23, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Zachary Boodoo - Graduate Student

Even on combined antiretroviral therapy (cART), people living with HIV (PLWH) experience a low level of viral replication that engenders a chronic inflammatory state and increases their risk to develop multiple types of vascular disease. Previous work by our lab has demonstrated platelet-monocyte complexes (PMCs) occur with greater frequency in PLWH due to aberrant platelet activation, and these complexes are associated with higher expression of monocyte activation markers, as well as pro-inflammatory CD16+ intermediate and non-classical monocyte (NCM) phenotypes. However, the fate of PMCs in the vascular disease microenvironment, and the platelet-induced transcriptional networks that lead to cellular dysfunction, are not well characterized.

Considering these unknown entities, we implemented a study cohort to investigate the effects of chronic HIV infection on vascular disease (atherosclerosis). Participants were age-, sex-, and Reynolds risk score-matched and divided into four subgroups based on their HIV and AS status (HIV-AS-, HIV+AS-, HIV-AS+, and HIV+AS+) (n=32). Monocytes were isolated from participant PBMC or whole blood samples via flow-activated cell sorting (FACS) and analyzed by single cell RNA sequencing (scRNA-seq). Unbiased clustering revealed 10 monocyte subsets that were conserved across participants groups, two of which were identified as PMCs based on an enrichment of platelet-associated transcripts. Differential gene expression (DGE) analysis of PMCs in PLWH and AS together compared to people living with AS (PLWAS) alone revealed an upregulation of genes involved inflammatory responses (antigen processing and presentation, chemokine signaling pathway), lipid metabolism (arachidonic acid metabolism, ABC transporters, alpha linoleic acid metabolism), and cardiovascular function (cardiac muscle contraction, arrhythmogenic right ventricular cardiomyopathy). Mass spectrometry of participant plasma samples revealed differentially abundant proteins associated with vascular disease processes. Stabilin-1, a macrophage and endothelial cell scavenger receptor with atheroprotective effects, and angiopoietin-like 4 (ANGPLT4), a pro-resolving factor in an inflamed intima environment, were less abundant or entirely absent in the plasma of HIV+AS+ participants compared to those who are single-afflicted or healthy controls. Myotrophin, a myocardial hypertrophy-inducing factor elevated in people who have experienced heart failure, and serum amyloid A2, a well-characterized local mediator of atherosclerosis and vascular dysfunction, were elevated in HIV+AS+ participants.

Oxidized lipoprotein (oxLDL), a key mediator of atherosclerosis, has been demonstrated to incur epigenetic changes in monocytes that alter its response to future inflammatory stimuli. To determine the effect of platelet interactions on this trained immunity paradigm, monocytes and collagen-activated platelets were cocultured for seven days with or without oxLDL, and stimulated with LPS at day six. Flow cytometric analysis of monocyte-derived macrophages revealed that platelet interactions decreased CD36 (scavenger receptor) and CD14 expression, and increased expression of antigen-presentation molecule CD86. CD40 expression was similar between non-PMCs and PMCs, but LPS-stimulation reduced expression in PMCs relative to non-PMCs. Collectively, these results demonstrate that platelets alter monocyte-macrophage phenotypes, and PMC gene signatures in PLWH and AS are proinflammatory. In-depth understanding of platelet-mediated monocyte dysfunction in HIV infection can pave the way to develop potential therapeutic approaches to address viral-associated vascular disease and related comorbidities

 Sep 19, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisors: Meera Singh, PhD and Juilee Thakar, PhD

Yuchang Liu - Graduate Student

Antibiotic resistance has been an increasing global health issue, and the spreading of antibiotic resistance will lead to the emergence of multi-drug resistance bacteria. While conjugation is one of the most important ways of spreading antibiotic resistance, separate plasmid transfer events always exhibit different efficiencies. Right now, the literature consensus believes that recipient strains will not play a large role in dictating conjugation efficiencies, but all the previous studies just used KO or mutant libraries of the same parent strain, which can only induce low genetic diversity. Hence, there is a gap in our mechanistic understanding of recipient-specific features that impact conjugation efficiency. However, due to the genetic differences between different strains, they will probably build up different conditions and barriers for the plasmids, and thus show different abilities to receive the plasmids. In addition, we collected more than 30 drug-susceptible Klebsiella pneumoniae isolates, and found their abilities to receive plasmids are significantly different. We aim to explore the factors that determine an optimal plasmid recipient in the genetic aspect. Currently, we have found several potential gene clusters that might contribute to the high conjugation efficiency phenotype through a functional genomic screen. We also have verified that the insertion of some of these potential genes will make a difference in the conjugation efficiency. In the future, we will also try to find out the genes that contribute to the low conjugation efficiency.

 Sep 12, 2024 @ 12:30 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Allison Lopatkin, PhD

Chenghao Wang - Graduate Student

Toxoplasma is a common intracellular parasite that can infect almost all nucleated cells. Innate immune recognition of this pathogen leads to the production of chemokines and IL-12, which are crucial for host resistance to the parasite. We have previously defined the key steps involved in T. gondii recognition in the mouse system and identified TLR11 as a major innate immune sensor that recognizes T. gondii profilin and triggers a potent MyD88-dependent IL-12 response essential for host resistance.

Additionally, we recently revealed that the production of CCL2 by mouse and human cells is central to regulating immunity to T. gondii. We and others have shown that this response can be induced via TLR11-dependent and independent mechanisms, with the TLR11-independent release of the human alarmin S100A11 contributing to CCL2 production. In my work, I identified that, in addition to proteins, the release of lipids from T. gondii-infected human cells plays a role in the induction of CCL2 by monocytes. Furthermore, different T. gondii virulence factors may influence the parasite's recognition by human cells and the lipid-mediated induction of CCL2. The current work is focused on the molecular mechanisms responsible for the release of lipids during T. gondii infection of human cells.

 Sep 12, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Felix Yarovinsky, MD

Imtiaz A. Khan, PhD - Professor of Microbiology, Immunology, and Tropical Medicine, George Washington School of Medicine & Health Sciences

Toxoplasma gondii is a major food-borne illness that causes severe disease in humans, especially newborns and immunocompromised individuals. CD8 T cell immunity is critical for keeping chronic infection under control, During later phases of chronic infection, CD8+ T cells develop exhaustion which compromises long-term immunity against the parasite, causing reactivation of latent infection. Maintenance of functional memory CD8 population is highly essential for host survival and it is critical to understand the mechanism by which this response can be achieved. Data from our laboratory demonstrates that CD8 T cell response is comprised of heterogenous population including one effector and three memory populations. The process is complex and individual contribution of memory subsets in the generation of effector response need to be studied.

 Sep 09, 2024 @ 12:00 p.m.

 Medical Center | Upper Aud. (3-7619)

Host: Felix Yarovinsky

Lauren Paddock - Graduate Student

Obesity-related type 2 diabetes (obesity/T2D) is associated with a dysbiotic gut microbiome, chronic inflammation, and impaired adaptive and innate immunity that increases the risk of severe bacterial infections. Previous research in our lab has shown that supplementation with the dietary fiber oligofructose (OF) reduces the severity of Staphylococcus aureus osteomyelitis in a mouse model of obesity/T2D, as well as partially correcting the gut microbiota to a homeostatic state with an increase in beneficial bacteria. However, our understanding of the mechanisms by which modifications of the gut microbiota and diabetic microenvironment alter host infection responses are limited. Metabolite analysis of the oligofructose supplemented obese/T2D mice revealed elevated levels of polyamines, immunomodulatory metabolites synthesized by the gut microbiota and the host. Although polyamines are a common metabolite of the gut microbiota, the bacterial community that contributes to polyamine biosynthesis remains unclear. We found that the increased levels of polyamines locally in the gut and systemically in the plasma correlated with a higher abundance of Bifidobacterium pseudolongum, indicating that this member of the gut microbiota may contribute to increased production of polyamines. Other investigators have shown that Enterococcus faecalis contributes to production of polyamine through a symbiotic association with other gut bacteria and integration of polyamine biosynthesis pathways across multiple taxa. To identify additional bacteria in the oligofructose supplemented mice that contribute to polyamine biosynthesis, we isolated representative bacterial taxa from mouse fecal material and screened for production of polyamines. Isolates from each of four taxa, B. pseudolongum, Lactobacillus johnsonii, Staphylococcus epidermidis, and Enterococcus faecalis produced varying levels of polyamines, suggesting strain specific polyamine biosynthesis. We have sequenced the complete genomes of these isolates to further determine the pathways and potential regulatory mechanisms of polyamine biosynthesis in these species. Further in vitro co-culture experiments, along with untargeted metabolomic analyses, will identify potential symbiotic interactions between these species that contribute to host response and coordinated production of polyamines and other metabolites that modulate the immune response to infection.

 Sep 05, 2024 @ 12:30 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Steven Gill, PhD

Thomas Wilson - Graduate Student

A recent resurgence of poxvirus infections around the world has renewed the need for improved vaccines and anti-viral treatments for these viruses. Clade-1 Monkeypox has been named a public health emergency with an increase in spread outside of Africa. This resurgence highlights major knowledge gaps in our understanding of this family of medically important viruses. Among these is the lack of a widely accepted and confirmed cellular receptor(s). With multiple receptors proposed, a more direct approach is required. Here, we propose the use of yeast display to interrogate putative proteins as receptors for the prototypical poxvirus, vaccinia. Yeast do not natively interact with vaccinia virus and carry out post-translational modifications that are similar to mammalian cells. Currently we have integrated several potential receptors into a yeast display system and are verifying their expression and native conformation. This will allow us test fluorescent virion binding via yeast pull-downs. Flow cytometry will be used to confirm binding and quantify the affinity of any potential interactions. Identification of cellular receptors for poxviruses should allow for the development of better drugs and antibodies that target specific virion proteins that are involved in poxvirus binding and entry.

 Sep 05, 2024 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Brian Ward, PhD

Jennifer Nicholson - Graduate Student

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting multiple organ systems. Lupus nephritis (LN) is one of the most common and severe clinical manifestations of SLE, resulting in kidney damage and impaired kidney function. Currently, therapies for SLE are aimed at reducing immune activation rather than treating chronicity and tissue damage. Sodium glucose cotransporter 2 (SGLT2) inhibitors are a promising treatment option to address this unmet need. Originally approved for use in type 2 diabetes, SGLT2i have improved renal outcomes in patients with chronic kidney disease from multiple etiologies. Interestingly, SGLT2i have recently been shown to reduce cellular senescence in the kidneys of diabetic mice. However, the mechanisms underlying the reno-protective effects of SGLT2i are still unclear and have yet to be investigated in LN. Preliminary data from our lab shows a decrease in kidney fibrosis, autoantibody secreting cells, and cystatin C—a marker of kidney damage—in lupus-prone mice after treatment with SGLT2i. Recently, cellular senescence has been described in the LN kidney. Elevated levels of p16INK4a, a cell cycle arrest protein frequently used as a marker of senescence, were detected in kidney tissues of human LN patients and correlated with disease severity. Additionally, we have demonstrated an increase in p16INK4a, γH2AX, and other senescence markers in the kidneys of NZB/W lupus-prone mice. There are several key questions remaining to be addressed, including the relationship between senescence and disease severity, cell types affected, and contribution to disease pathology. To begin to address these questions, we will leverage existing kidney tissues from NZB/W mice at a variety of ages and disease stages and utilize immunohistochemistry to detect the presence of different senescence markers. NZB/W mice will be treated with SGLT2i, and the impact on senescence markers, kidney damage, and immunopathology will be evaluated via IHC and qPCR. Our study may help define the role of cellular senescence in LN and support the use of SGLT2i as a novel therapeutic option in LN.

 Aug 29, 2024 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Microbiology and Immunology Student Seminar
Advisor: Jennifer Anolik, MD, PhD

Amelia M. Knudsen-Clark, MS - PhD Candidate

 Aug 26, 2024 @ 12:00 p.m.

 Medical Center | K-207 (2-6408)

Host: Advisors: Brian J. Altman, PhD and Minsoo Kim, PhD

Tentative Itinerary

Please RSVP by Friday August 9^th

 Aug 23, 2024 @ 8:00 a.m.

 Helen Wood Hall | Aud 304

Tara Vrooman - PhD Candidate, Immunology, Microbiology and Virology PhD Program

 Jul 30, 2024 @ 10:00 a.m.

 Medical Center | K-207 (2-6408)

Host: Advisor: Scott Gerber, PhD

Joshua W. Modell, PhD - Assistant Professor of Molecular Biology & Genetics, Johns Hopkins University School of Medicine

CRISPR-Cas systems provide bacteria with adaptive immunity against bacteriophages and other foreign genetic elements. However, there is a growing appreciation that overexpression of CRISPR-Cas components is toxic in both their native hosts and heterologous systems for gene editing. In this seminar, I will discuss the S. pyogenes CRISPR-Cas9 system and describe how it is (i) transcriptionally repressed to mitigate autoimmune toxicity in the absence of phage and (ii) rapidly induced in the presence of phage to promote bacterial survival.

 Jun 10, 2024 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Dept. Microbiology & Immunology Seminar Series and Andrew Varble, PhD

Kala Hardy, MS - PhD Candidate, Immunology, Microbiology and Virology PhD Program

 Jun 10, 2024 @ 10:00 a.m.

 Medical Center | K-207 (2-6408)

Host: Advisor: Toru Takimoto, PhD

Anushka Dongre, PhD - Assistant Professor, Department of Biomedical Sciences, Department of Microbiology and Immunology Cornell University

Although immune checkpoint blockade therapy has generated dramatic responses in certain cancers, the response of breast tumors has been largely limited. By establishing novel, preclinical murine models of more-epithelial or more-mesenchymal breast tumors, we demonstrate that the cellular plasticity of breast cancer cells can itself be an important determinant of responsiveness to such therapy. Moreover, interrupting certain signalling channels specifically associated with mesenchymal cancer cells, can potentiate the effects of checkpoint inhibition leading to the elimination of more-mesenchymal breast tumors. Thus, our work highlights the prospect of using the polarization of carcinoma cells on the epithelial-mesenchymal spectrum as a surrogate marker for predicting responses to immune checkpoint blockade therapy.

 Jun 03, 2024 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Dept. of Microbiology & Immunology Seminar Series and Scott Gerber, PhD

Alex Pomakov, MD - Fellow, Univ. of Rochester Infectious Diseases Division

Meeting ID: 912 6958 5749

Passcode: 258684

 May 14, 2024 @ 11:45 a.m.

Jennifer Nayak, MD - Associate Professor, Department of Pediatrics, Infectious Diseases

 Apr 26, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Felix Yarovinsky, MD - Professor, Department of Microbiology and Immunology, Center for Vaccine Biology and Immunology

 Apr 19, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Joon Seok Park, Ph.D. - Instructor in Immunology, Harvard University

It has become clear that commensal microbes play important roles in maintaining immune homeostasis while responding robustly to foreign insults. A fascinating illustration of this process is the impact of gut microbes on the body’s immune defense against tumors located beyond the intestinal tract. My recent research revealed a novel underlying immune mechanism by which gut microbes promote anti-tumor immunity and opened novel research avenues for the exploration of cancer therapies. However, it remains enigmatic how gut-confined microbes can impact immune responses to distal tumors. Additionally, the precise context in which the gut microbe-mediated immune modulation become crucial in governing systemic immunity is poorly understood. My laboratory will determine 1) the immunomodulatory mechanisms mediated by commensal microbes in cancer and chronic viral infection 2) the roles of microbial lipids in innate signaling in the tumor microenvironment (TME) and 3) the mechanisms of crosstalk between the TME and gut microbiota. My research program will clarify the promise and limitations of cancer immunotherapy using gut microbiota and address why some cancers depend on gut microbiota and others do not. In addition, this work will tackle how specific gut microbes modulate systemic antiviral immunity leveraging our extensive information obtained from tumor studies, providing a unique direction to find the underlying mechanisms. This will guide the development of novel cancer immunotherapies and new approaches to improve vaccines.

 Apr 18, 2024 @ 4:00 p.m.

 Kornberg Medical Research Building | 3.9624

Paul Bohjanen, MD, PhD - Professor, Department of Medicine, Infectious Diseases

 Apr 12, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Shawn Murphy, PhD - Associate Professor, Departments of Obstetrics & Gynecology and Microbiology & Immunology

 Apr 05, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Yunlong Zhao, PhD - Assistant Project Scientist, School of Biological Sciences, University of California San Diego

Cancer immunotherapy is revolutionizing the way we fight disease, but many patients don't reap its full benefits. My research focuses on understanding how immune cells called T cells communicate with cancer cells and other immune cells. Typically, studies have focused on how receptor signals pass directly between cells. However, I also study how signals are exchanged in the same cell. These "internal conversations" can powerfully shape how T cells fight tumors. My work has shown that they can make T cells more effective against cancer. By carefully mapping how T cells talk to themselves, especially in cutting-edge therapies like adoptive cell therapy, I aim to uncover hidden targets for improvement. This knowledge could usher in a new era of immunotherapy where these incredible treatments work for even more patients.

 Mar 28, 2024 @ 4:00 p.m.

 Kornberg Medical Research Building | 3.9624

Clive Zent, MD - Professor, Department of Medicine, Hematology/Oncology

 Mar 22, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Kristin Scheible, MD - Associate Professor, Department of Pediatrics, Neonatology & Microbiology and Immunology

 Mar 15, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Kirsi Jarvinen-Seppo, MD, PhD - Professor, Department of Pediatrics, Pediatric Allergy/Immunology

 Mar 08, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Joshua Anzinger, PhD - Senior Lecturer, Department of Microbiology
The University of the West Indies
Head of Virology, Consultant Virologist and
Director of Jamaica Affiliate Global Virus Network

Viral epidemics have become increasingly common worldwide. In Jamaica, viral epidemics have occurred every 2-3 years over the past decade, all on the backdrop of existing retrovirus epidemics. This seminar will provide a research-driven overview of recent viral epidemics in Jamaica and describe the capacity building approach to facilitate more effective research responses to future viral epidemics.

 Feb 29, 2024 @ 1:15 p.m.

 Medical Center | Lower Adolph Aud. (1-7619)

Host: Jacques Robert, PhD

Minsoo Kim, PhD - Professor, Department of Microbiology and Immunology, Center for Vaccine Biology and Immunology

 Feb 23, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Brian Altman, PhD - Assistant Professor, Department of Biomedical Genetics

 Feb 16, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Craig Morrell, DVM, PhD - Professor, Department of Medicine, Aab Cardiovascular Research Institute

 Feb 09, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Ruchira Singh, PhD - Associate Professor, Dean's Proffesor of Ophthalmology, Biomedical Genetics, Center for Visual Science, and member of UR Batten Center

 Jan 31, 2024 @ 4:00 p.m.

 Kornberg Medical Research Building | G.11211 (CVRI Conf. Rm)

Host: Aab Cardiovascular Research Institute (CVRI) University of Rochester CVRI Seminar Series

Jacques Robert, PhD - Chair, Microbiology & Immunology

 Jan 26, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Angela Branche, MD - Associate Professor, Department of Medicine, Infectious Diseases

 Jan 19, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624