Center Events

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

 Apr 26, 2024 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-6924

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

 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

Regina Rowe, MD, PhD - Assistant Professor, Pediatrics/Infectious Diseases

 Dec 08, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Stephen Hammes, MD, PhD - Professor, Medicine/Endocrine/Metabolism

 Nov 17, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Ian Stone - PhD Candidate, Immunology, Microbiology and Virology PhD Program

The elderly population are more susceptible to viral infections, in part due to increased dysregulation of immune responses, which are associated with increased age. Uncovering shared effector mechanisms between processes that regulate healthy aging and viral infection protection could represent novel pharmaceutical targets to decrease mortality rates. 

Caenorhabditis elegans (C. elegans) is an excellent model system for aging research, given its brief lifespan, short generation time, and high homology to human disease genes. Interestingly, C. elegans lack professional immune cells, allowing the study of innate immunity in isolation. Orsay virus (OV) is a natural viral pathogen of C. elegans, allowing for the genetic analysis of host-virus interactions in this model organism. I found older animals have decreased activation of innate immune pathways in response to OV infection and increased viral load over the course of infection compared to younger animals, suggesting they cannot adequately regulate viral replication. 

The mechanistic target of rapamycin (mTOR) is a major longevity pathway that controls aging and responds to cellular stress. mTOR forms two complexes, but mTORC1 has an important role in combating viral replication; downstream adaptive responses including autophagy and protein translation have been implicated in cellular stress responses to viral replication. I found that knockdown of TOR improved C. elegans resistance to OV infection, but the mechanisms underlying this resistance are still unknown. By continuing my study of requirements for mTOR-driven protection, I will be able to study the potential of mTORC1 as a therapeutic target for improving healthy aging and viral protection.

 Nov 16, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Andrew Samuelson, Ph.D. and Brian Ward, Ph.D. - Advisors

Gowri Muthukrishnan, PhD - Assistant Professor, Orthopaedics/CMSR

 Nov 10, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Jennifer Anolik, MD, PhD - Professor, Medicine/Allergy, Immunology & Rheumatology

 Nov 03, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Jeremiah Johnson, PhD - Associate Professor of Microbiology, University of Tennessee

Special Faculty Candidate Seminar

Campylobacter jejuni is the leading global cause of bacterial-derived gastroenteritis and induces neutrophil extracellular traps (NETs), which are structures comprised of DNA and antimicrobial proteins that can restrict pathogen growth and dissemination during infection. In a recent study, we identified a sirtuin encoded by C. jejuni that is secreted from the bacterium into human neutrophils where it associates with and deacetylates host histones to promote neutrophil activation and NET production. Using the murine model of campylobacteriosis, we found that a mutant of this sirtuin efficiently colonized the gastrointestinal tract, but was unable to induce cytokine production, gastrointestinal inflammation, and tissue pathology. These results suggest that secreted bacterial sirtuins are a previously unreported class of effector and that bacterial-mediated modification of host histones is responsible for the inflammation and pathology that occurs during campylobacteriosis.

Further, while NETs are efficient at limiting bacterial burden at the site of infection, numerous pathogens encode nucleases that degrade NETs to evade their antimicrobial effects. Because we found that C. jejuni viability is not impacted by human NETs, we hypothesized and found that unidentified C. jejuni nucleases promote the degradation and evasion of human NETs. Since the determinants required for C. jejuni nuclease production are poorly understood, we conducted a screen and identified a DNA glycolyase, called MugA, that promotes degradation and evasion of NETs. In addition, MugA-dependent NET degradation products promoted host inflammation through NLRP3-dependent inflammasome activation in adjacent macrophages. As such, while MugA assists the bacterium in evading NET killing, it promotes host inflammation. As a result, we found that a mugA mutant inconsistently colonizes and causes reduced inflammation when compared to wild-type-infection. These results suggest that nuclease-targeted therapeutics may be efficacious at reducing pathogen burden and disease within infected hosts.

 Nov 02, 2023 @ 2:30 p.m.

 Medical Center | Lower Adolph (1-7619)

Host: Department of Microbiology & Immunology

Andy Phan - PhD Candidate, Immunology, Microbiology, and Virology PhD Program

Human immunodeficiency virus 1 (HIV-1) is a pathogen responsible for an ongoing global epidemic, for which there is no curative therapy or protective vaccine.  Although there exists antiretroviral therapy (ART) which is effective in suppressing further HIV-1 replication, the virus cannot be eliminated from the patient, and cessation of ART would lead to rebound of viral replication.  The major obstacle towards an HIV-1 cure is the persistence of replication-competent viral DNA.  In infected cells, latent HIV-1 DNA is transcriptionally silenced and not susceptible to the host immune system or antiretroviral drugs.  Latency is commonly associated with the deposition of repressive epigenetic modifications and removal of active epigenetic modifications, which occurs through interactions with cellular proteins, but the exact mechanisms for silencing of viral DNA are not well understood.

By employing a CRISPR-Cas9 knockout screen, we assessed host factors to determine their potential in the silencing of viral gene expression, and identified the cohesin complex subunits SMC1A, SMC3, and RAD21 as cellular proteins responsible for silencing of HIV-1 DNA.  We show that depletion of these host factors leads to a significant increase in viral DNA expression.  We also assess the ability of Vpr, an HIV-1 accessory protein linked to enhancing viral gene expression, to counteract host-mediated silencing.  Our current experiments explore the mechanisms by which the cohesin complex may promote compaction of viral chromatin and therefore contribute to decreased viral gene expression, and the ability of HIV-1 to antagonize this silencing.  Expansion in this area of HIV-1 research will contribute to the progress of novel therapies to fully eliminate latent DNA in infected cells.

 Nov 02, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Yiping Zhu, PhD - Advisor

Ben Frisch, PhD - Assistant Professor, Pathology & Laboratory Medicine

 Oct 27, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Adam Geber - PhD Candidate, Medical Scientist Training Program (MSTP)
Immunology, Microbiology and Virology PhD Program

The immune system is classically divided into two categories: innate and adaptive, where the former responds rapidly and nonspecifically and the latter does so more slowly, precisely, and with greater speed and specificity over time. These conceptual distinctions are most appropriate for adult humans, who have a substantial repertoire of mature naïve lymphocytes that can establish immunological memory to protect against reinfection. Because the infant immune system continues to develop after birth and does not yet have an archive of memory cells, it must be capable of rapid and often nonspecific responses to signals of danger and damage. T cells are crucial to proper functioning of the adaptive immune system and are responsible for recruiting and coordinating immune cells, shaping future responses, and directly killing infected or cancerous cells. CD8+ T cells are canonically known for their cytolytic functions but can also produce cytokines under certain inflammatory conditions. During the last two decades an array of lymphoid immune cells have been described as having innate-type functions and/or a strongly restricted capacity for recognizing foreign antigens. More recently, we have found evidence for a subset of CD8+ T cells that arise in utero during the second trimester, persist variably into adulthood, and behave in an innate-like manner. We report the initial flow cytometric characterization of the phenotype and function of putative fetal innate-like CD8+ T cells (FITs) derived from cord blood mononuclear cell samples.

 Oct 26, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: David Topham, PhD - Advisor

Suryaram (Rham) Gummuluru, PhD - Professor & Vice-Chair, Department of Virology, Immunology & Microbiology, Director, Graduate Medical Sciences Immunology Training Program (ITP) Investigator, National Emerging Infectious Diseases Laboratory (NEIDL) Co-Director, Developmental Core, Providence/Boston Center for AIDS Research (Prov/Bos CFAR) Boston University

 Oct 23, 2023 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Steve Dewhurst, PhD

Juilee Thakar, PhD - Associate Professor, Microbiology & Immunology

 Oct 20, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Ankit Dahal - Graduate Student, Immunology, Microbiology, and Virology Ph.D. Program

Cancer deaths is the 2nd leading cause of mortality worldwide, and the total number of cancer related deaths is anticipated to only increase. Emerging evidence suggests that the presence of polymorphonuclear (PMN) myeloid derived suppressor cells (MDSCs) with neutrophil-like phenotypes and morphologies play a major role in adverse clinical outcomes due in part to their contribution in establishing immunosuppressive tumor microenvironment (TME). Despite recent advances in our understanding of MDSC phenotypes and characteristics in the TME, the underlying molecular mechanisms by which classical neutrophils differentiate into MDSC within the TME remails largely unknown. 

To investigate the microenvironmental cues that regulate PMN-MDSC differentiation at the tumor site, we established several in vitro co-culture systems using multiple human and murine cancer cells and 3D spheroid conditions. With live cell migration microscopy, we first showed that neutrophils actively swarmed into the pancreatic cancer spheroids and stayed active for an extended period in the tumor. We further found that cancer cell culture supernatant significantly extended neutrophil survival and successfully differentiated neutrophils into MDSCs that exhibited increased arginase and suppressed CD8 cytotoxicity and proliferation. To identify the major macromolecules in the supernatant mediating MDSC differentiation, we selectively inactivated and depleted different classes of macromolecules and discovered that the loss of lipid signal from the cancer supernatant completely abrogated the ability of PMNs to differentiate into MDSCs. To further identify the specific lipid molecules mediating such effects, we utilized LC-MS lipidomic analysis to screen for major lipids secreted by both murine and human cancer cells and identified several arachidonic acid and other inflammatory lipid molecules including platelet activating factor (PAF). Meta transcriptional and survival analysis of human PDAC cancer highlights a strong negative association between the expression of PAF generating enzyme, LPCAT2, and patient survival, suggesting that PAF may be implicated in cancer progression and growth. Given that PAF is a strong neutrophil activator, we hypothesize that PAF mediated signaling may promote the differentiation of MDSCs in pancreatic cancer. 

 Oct 19, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Minsoo Kim, PhD - Advisor

Joseph E. Peters, PhD - Professor and Chair, Department of Microbiology
Cornell University

Transposon Tn7 and Tn7-like elements are notable for the control they exercise over where transposition events are directed. In these diverse elements one integration pathway recognizes a highly conserved attachment (att) site in the chromosome, while a second pathway specifically recognizes mobile plasmids that facilitate transfer of the element to new hosts. There has been a flood of recent work with these systems, including the discovery of five independent events were CRISPR-Cas systems have been coopted for natural guide RNA-directed transposition. New families of Tn7-like elements also include a variety of novel att sites in bacterial chromosomes where genome islands can form in important pathogens like Acinetobacter baumannii. I will present work from my lab that is expanding our understanding of Tn7-like elements, broadening our view of how genetic systems are repurposed and indicating potential new tools for genome modification and genomics.

 Oct 16, 2023 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Andrew Varble, PhD

Tim Flerlage, MD - Assistant Professor, Pediatrics/Infectious Diseases

 Oct 13, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Hansol Im, PhD - Postdoctoral Fellow, Laboratory of Carlos J. Orihuela
University of Alabama at Birmingham

Streptococcus pneumoniae (Spn) is a Gram-positive bacterium and the leading cause of community-acquired pneumonia. In most instances, Spn resides in the nasopharynx asymptomatically. However, in infants or elders, those who are immunocompromised, or when a viral infection has damaged the airway, this opportunistic pathogen can cause infection of the lower airway and bloodstream. Annually, more than ten million individuals are hospitalized globally due to Spn infection, and as a result, hundreds of thousands die despite appropriate antimicrobial therapy. Thus, a better understanding of Spn-host interaction merits additional research to identify new therapeutic targets. In this series of studies, we observed that the physiology and virulence expression of the bacteria were highly dependent on where they were located within the host and surrounding carbon availability. Carbon metabolism and its alteration according to carbon availability are critical in determining the physiology and survival of Spn in the host. We evaluated carbon metabolic pathways involved in redox balance and its impact on downstream bacterial physiology and virulence phenotype. We found that NAD(H) redox balance during fermentation was vital for Spn energy generation, capsule production, in vivo fitness, and survival under antibiotic stresses. Moreover, targeting the NAD(H) metabolic pathway enhanced the susceptibility of multidrug-resistant Spn to antibiotics and prevented invasive disease in an animal infection model. Together, our results indicate carbon metabolism pathways are de novo targets for antibiotic development and a novel strategy to combat multidrug-resistant pathogens. Subsequently, better resolution in bacterial metabolic shifts during the course of disease will expand our understanding of the host-pathogen interactions at the foundation of Spn’s ability to cause disease, which can be valuable targets for novel therapeutics.

 Oct 12, 2023 @ 2:00 p.m.

 Medical Center | Lower Adolph Auditorium (1-7619)

Justin Brennan - Graduate Student, Immunology, Microbiology and Virology PhD Program

Defective viral genomes (DVGs) are truncated derivatives of their parental viral genomes unable to replicate without a full-length helper virus. DVGs have been observed in most RNA viruses and play critical roles in viral pathogenesis and evolution. During respiratory syncytial virus (RSV) infection, the copy-back type of DVGs (cbDVGs) potently induce the antiviral response. RSV is among the most consequential agents of pediatric respiratory illness and RSV cbDVGs correlate with antiviral responses in children; thus, cbDVGs are candidates for antivirals and vaccine adjuvants. Currently, little is known about the mechanisms of cbDVG generation or species-specific functions of cbDVGs, limiting our ability to use cbDVGs to mitigate viral pathogenesis. Our lab has shown that RSV cbDVG generation is not a stochastic process and identified three genomic “hotspots” (R1, R2 and R3) mediating the formation of cbDVGs. Moreover, the introduction of a poly-U mutation into R1 reduced its role in cbDVG formation, demonstrating that cbDVG generation is genetically manipulable. Here, our previous work was expanded on by generating a mutant virus with a similar mutation in R2 (10U). cbDVGs were enriched in WT and 10U viruses by high MOI passaging. Strikingly, the 10U virus had a two-passage delay in cbDVG generation compared to WT and this delay was recapitulated in a primary pediatric lung epithelial cell system. RNA-seq analysis of the cbDVG populations enriched in the WT and 10U viruses showed that the frequency of R2 cbDVGs was largely reduced by the 10U mutation, with R3 becoming the major rejoin hotspot. To examine the species-specific functions of R2 and R3 cbDVGs, the major WT (WT 1887) and 10U (10U 1563) cbDVGs were selected for further analysis. Compared to WT 1887, 10U 1563 had enhanced replication kinetics and, when transfected as naked RNA, induced significantly more interferon and ISG expression per cbDVG. Interestingly, this difference was minimized in the presence of the RSV nucleoprotein. Overall, these data support our previous findings and establish that various RSV cbDVG species have distinct replication kinetics and immunostimulatory capacities, and implicate the RSV nucleoprotein in mediating these functions.

 Oct 12, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Yan Sun, PhD - Advisor

Kathryn M. Kauffman, PhD - Assistant Professor, Department of Oral Biology School of Dental Medicine University at Buffalo

Viral predators and partners of bacteria (called phages) are present in essentially all microbial communities and shape their structure and function. Yet, understanding and predicting the impacts of phages on microbial communities remains a challenge. In this talk I highlight our work addressing this challenge through a focus on resolving phage-bacteria interactions in two model systems. In our marine model we focus on Vibrio, fast growing heterotrophs; establishing a collection of >250 phage-bacteria pairs, sequencing all genomes, and generating a complete all-by-all matrix of killing interactions. In our oral model we focus on Porphyromonas gingivalis, a keystone pathogen in periodontal disease; using bioinformatic approaches to investigate publicly available genomes. Take-aways include important considerations for development and deployment of phages in bioengineering, industry, and medicine, and a reminder that ecologically important phages can be missed even in well-studied host systems. For more details about our work please visit https://kauffmanlab.org/

 Oct 09, 2023 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Andrew Varble, PhD

Jennetta Hammond, PhD - Assistant Professor, Neurology/Neuroimmunology

 Oct 06, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Kelli Connolly, PhD - Associate Research Scientist, Yale School of Medicine

We do not know if the lack of responses to checkpoint blockade immunotherapy (CPI) in some NSCLC subtypes is due to a lack of therapy-responsive T cells, or whether it is caused primarily by T cell-unrelated factors. Recently, utilizing a model of KP NSCLC, we discovered that a stable reservoir of TSL are maintained in tumor-draining lymph nodes (TDLN) throughout disease progression and migrate to the tumor over time, preserving the intratumoral CPI response. We hypothesize that TSL reservoirs are maintained within tdLNs of poorly responsive subtypes of NSCLC, such as KL, and that these cells can be leveraged to improve CPI responsiveness. To test this, I have developed genetically engineered mouse models of autochthonous KP, KPL, and KL NSCLC with inducible expression of a shared tumor neoantigen, thus allowing for direct comparisons of tumor-specific T cell responses in the context of these commonly occurring co-mutations.

NOTE: Dr. Connolly received her Ph.D. Degree in 2017 from UR in Microbiology and Immunology

 Oct 02, 2023 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Scott Gerber, PhD

Shannon Hilchey, PhD - Research Assistant Professor, Medicine/Nephrology

Bagels & Coffee available at 8:30 am in KMRB 3-9623

 Sep 29, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3.9624 East

Paige Lawrence, PhD - Professor, Department of Environmental Medicine

Breakfast Items & Coffee will still be available at 8:30 am in KMRB 3-9623

 Mar 31, 2023 @ 9:00 a.m.

M. Kerry O'Banion, MD, PhD - Professor, Department of Neuroscience

 Mar 24, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Dave Topham, PhD - Professor, Center for Vaccine Biology & Immunology

Meeting ID: 976 3491 7477
Passcode: 664735

 Mar 17, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

The 2023 RNA Institute Symposium will be held March 16-17th at the University at Albany, in collaboration with the UR Center for RNA Biology.

Call for Abstracts

We are pleased to announce our upcoming 2023 Annual RNA Institute Symposium hosted by the RNA Institute at the University at Albany in collaboration with the RNA Center for Biology at the University of Rochester. This year's meeting will focus on strengthening connections between academia and industry, hosting invited speakers from New York State Biotech and Pharma Industries as well as academia.

Event Highlights

Speakers from NY Biotech & Pharma Industries and Academia
Networking Opportunities with Industry Scientists

Trainee Talks
Lightning Talks of Selected Posters

Poster Sessions
Cash Awards for trainee talks and Posters

Abstract submission and registrations are now open.

Abstract submission closes by February 3, 2023. Feel free to pass along the attached advertisement to your friends and colleagues.

Submit your abstract and register at the link below

Register Today

 Mar 16, 2023 @ 9:00 a.m.

Jerry Workman, PhD - Investigator; Director of Postdoc Affairs, Stowers Institute for Medical Research, Kansas City, MO

Our Keynote Retreat Speaker this year is Dr. Jerry Workman, Investigator; Director of Postdoc Affairs, Stowers Institute for Medical Research, Kansas City, MO. His talk title is “Signaling through Chromatin for Transcription and Metabolism”. His host is Dr. Jeff Hayes. The T32 Retreat this year will be co-sponsored by Graduate Women in Science (GWIS) and a supplement to the NIH NIGMS T32 in Cellular, Biochemical and Molecular Sciences.

New this year, there will be a Wellness and Resilience Panel following the Keynote, from 3:15 – 4:15 pm, moderated by Dr. Jeff Hayes. The featured panelists are:

• Brigid Cahill, PhD, Director, University Counseling Center,; Associate Professor of Clinical Psychiatry, University of Rochester
• Kermin Martínez-Hernández, PhD, Principal Facilitator, Center for the Improvement of Mentored Experiences in Research (CIMER); Associate Professor, Department of Chemistry, St. John Fisher University
• Susan H. McDaniel, PhD, Dr. Laurie Sands Distinguished Professor of Families & Health; Director, UR Medicine Physician Communication Coaching Program; Chief of Psychology and Director, Institute for the Family, Department of Psychiatry; Vice Chair, Department of Family Medicine, University of Rochester
• Adrienne Morgan, PhD, Vice President and Senior Associate Dean for Equity and Inclusion; Associate Professor, Department of Health Humanities and Bioethics; Associate Professor, Warner School of Education, University of Rochester.

 Mar 15, 2023 @ 1:00 p.m.

 Medical Center | Class of '62 Auditorium (G-9425)

Host: Dr. Jeffrey Hayes (co-sponsored by Graduate Women in Science GWIS)

Bing Li, PhD - Endowed Professor for Cancer Immunology, Professor of Pathology, Department of Pathology
University of Iowa, Iowa City, IA

 Mar 13, 2023 @ 12:00 p.m.

 Medical Center | WCI Formicola CR – 2-0727

Host: Minsoo Kim, PhD and Laura Calvi, MD

Ann Falsey, MD - Professor, Department of Medicine - Infectious Diseases

 Mar 10, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Simon Foster, PhD - West Riding Professor of Microbiology, The Florey Institute, School of Biosciences, University of Sheffield

The shape and integrity of bacteria are determined by cell wall peptidoglycan, a single macromolecule that surrounds the cell.  The synthesis of peptidoglycan is also the site of action of important antibiotics such as penicillin and vancomycin.  Thus bacterial viability, growth and division are dependent on the architecture and dynamics of this essential polymer.  We use a combination of high-resolution microscopy approaches to reveal peptidoglycan architecture, and its dynamics, using the major human pathogen Staphylococcus aureus as our primary organism.  Atomic force microscopy has demonstrated a complex, nanoscale peptidoglycan architecture in diverse species, which meets the challenges of maintaining viability and growth within their environmental niches, by exploiting the bioengineering versatility of the polymer.  The application of super-resolution fluorescence microscopy, coupled with new chemical probes has begun to reveal how the polymer is synthesized and hydrolysed during growth and division.  We have also used these approaches to determine the mode of action of antibiotics and molecular mechanisms of antimicrobial resistance.

 Feb 27, 2023 @ 12:00 p.m.

Host: Edward Schwarz, PhD

Jim McGrath, PhD - Professor, Department of Biomedical Engineering

Meeting ID: 976 3491 7477
Passcode: 664735

 Feb 24, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Taylor Jones - Graduate Student, Advisor: David Topham, PhD

Influenza and other respiratory viruses annually pose a global health and economic burden, leading to hospitalizations and even death. In order to formulate better treatments and vaccines, it’s imperative to understand the mechanisms that can reduce disease burden. Tissue- resident memory (Trm) CD8 T cells in the airway and lung are among the first line of defense against viral reinfection. The ability to provide surveillance at the primary site of infection distinguishes Trm from other CD8 memory T cells. Cell surface expression of CD69 has been used as a broad marker for Trm; however, the expression of integrins CD103 and CD49a distinguish subsets of Trm in the lung. CD49a binds to collagen IV, found in the basement membrane of the lung, and can be detected on CD8 T cells as early as 6-8 days post-infection. Functionally, CD49a has been implicated in Trm adherence, retention in the lung and airways, and motility within tissues. Anti-CD49a antibody blockade prior to secondary infection reduces Trm in the lung and is associated with increased mortality in mice. To further understand the functional relevance of CD49a in Trm, a transgenic OT-1 mouse-model was developed with a CD8 driven tamoxifen inducible CreERT2 recombinase crossed to loxP flanked Itga1 and tdTomato genes. Tamoxifen treatment leads to deletion loxP flanked genes, Itga1 (iCD8 Cre Itga1 tdTomato), which encodes CD49a. This model will be used to address how CD49a functions in tissue resident memory relating to motility, positioning within the tissues, and function. To test the model, splenocytes from iCD8 Cre Itga1 tdTomato mice were adoptively transferred into recipient B6 mice and infected the following day with X31-OVA influenza virus. Tamoxifen treatment was administered consecutively for 5 days beginning at day 32 post infection to trigger loss of CD49a. Flow cytometric analysis was done on the lungs, spleen, and mediastinal lymph node from these mice to measure changes in T cell localization. Treated mice had reduced CD49a+ memory CD8 T cells in the lung, suggesting the model works as expected. In the future, this model will be used to capture the cells’ potential to respond against secondary infection. The role of CD49a in motility within the airways will be examined by performing intravital multiphoton imaging of trachea using the adoptive transfer and infection model as before. The conditionality of this model will also allow us to prod the different time points that are essential for T cell memory. These experiments will help define the function of CD49a in local surveillance, retention, and antiviral immunity.

 Feb 23, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Tom Mariani, PhD - Professor, Department of Pediatrics - Neonatology

Meeting ID: 976 3491 7477

Passcode: 664735

 Feb 17, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Emily Britt - Graduate Student, Advisor: Steven Gill, PhD

Staphylococcus aureus is the most prevalent causative pathogen of prosthetic joint infections (PJIs). Obese-Type 2 Diabetics (Ob/T2D) are at an increased risk for post-operative infections due to immune dysfunction. Immune dysfunction is caused in part by gut microbiome dysbiosis that accompanies Ob/T2D. Microbial dysbiosis is characterized by altered community composition and abundance, which results in aberrant production of key gut microbe-derived metabolites. The balance of health and disease is dependent upon the synergistic interactions of these systems. Utilizing the Ob/T2D model, we can assess the contributions of both immune dysfunction and gut microbiome disturbances on infection severity. In our paradigm, we utilize a diet-induced Ob/T2D mouse model to study the impact of gut microbiome alterations on the immune response to infected surgical implants. Infections in Ob/T2D mice recapitulate increased severity seen in Ob/T2D humans compared to lean counterparts. Supplementation with dietary fiber oligofructose (OF) is known to alter the gut microbiome composition in humans and mice. We have shown that OF supplementation in our mouse model decreased infection severity in Ob/T2D mice. Targeted metabolomics revealed significantly increased polyamine output in Ob/T2D mice supplemented with OF. Supplementation with polyamines directly provided the same decrease in infection severity. I will perform dual-RNA sequencing of S. aureus-infected mouse tibia in our Ob/T2D model to determine the impact of dietary OF and polyamine supplementation on the host immune and S. aureus transcriptome responses in vivo. I will also complete in vitro assays to determine the mechanistic impacts of polyamines on macrophage gene expression and function as well as on S. aureus gene expression. I will present preliminary in vitro data that demonstrates the impact of polyamines on the expression of a key S. aureus host tissue adhesion factor. These experiments will give us better insight into how gut microbe-derived metabolites influence the immune response and ultimately the outcomes of infection, providing a glimpse at alternative methods to treat disease through modulation of host metabolism and immunity.  

 Feb 16, 2023 @ 12:30 p.m.

 Medical Center | K-307 (3-6408)

Zachary Boodoo - Graduate Student, Advisor: Meera Singh, PhD

As of 2021, approximately 38 million were living with HIV worldwide. The implementation and increased availability of combined antiretroviral therapy (cART) has both extended the lifespan and increased the quality of life for persons living with HIV (PLWH) while curtailing the rates of new infections (32% decline since 2010). These developments have made it possible for a significant population of HIV+ individuals to transition into middle and old age. Despite these advancements, PLWH exhibit an increased susceptibility to develop a vast number of comorbidities, which necessitates undertaking novel studies to address these concerns. One of these heightened disease states is cardiovascular disease, which is the subject of our research efforts.

Monocytes can be broadly classified into three subsets based on surface marker expression: classical (CD14+CD16-), intermediate (CD14+CD16+), and non-classical (CD14loCD16+). Although important in resolution of injury and homeostatic maintenance, non-classical monocytes, due to their pro-inflammatory phenotype, have been implicated in atherosclerosis (AS) by physically interacting with endothelial cells and contributing to plaque formation. Previous work done by our lab has demonstrated a higher percentage of these circulating non-classical monocytes in HIV+ individuals. Additionally, we observed a higher percentage of activated platelets in the same cohort, which have the propensity to form transient complexes with monocytes and induce their transition to the CD16+ subpopulation of interest. Platelet-monocyte complexes (PMCs) were found to be elevated in PLWH.

Platelets are the major source of circulating microparticles, which contain proteins, lipids, and RNA. Therefore, we hypothesize that platelet-monocyte complexes mediate efficient transfer of platelet-derived microparticles (PMPs), whose biomolecular contents induce monocyte maturation to the pro-inflammatory, CD16+ phenotype that is a major player in atherosclerosis and broader cardiovascular dysfunction. To investigate this, we will rely on human whole blood and plasma samples to isolate monocytes and platelet-derived microparticles, respectively, which were collected as part of a previously completed clinical study at the institution. Patients will be divided into subgroups based on HIV and AS status, with the latter determined by plaques revealed during carotid imaging data. Single-cell RNAseq and metabolic analysis will be performed on monocytes to construct a dynamic network model of gene expression that can identify differences in gene expression between patient groups. Concurrently, the miRNA and proteins enveloped within our isolated PMPs will be extracted and subject to small RNAseq and mass spectrometry analysis. miRNAs and proteins that differ between monocyte classes (platelet-complexed vs. non-complexed) or patient subgroups will be introduced into our network model to assess their ability to perturb monocytic signaling. Collectively, these sets of analyses will elucidate the impact of platelet-monocyte interactions on monocyte differentiation and function, and determine potential pathways that can be therapeutically targeted to prevent and treat AS.

As a preliminary experiment, platelet-derived microparticles were isolated from human plasma samples and incubated with both primary monocytes or U937 cells (a pro-monocytic cell line). Flow cytometry analysis demonstrated changes in cell surface marker expression between control and PMP-treated cells, however additional replicate experiments are needed to confirm these observations. 

 Feb 16, 2023 @ 12:00 p.m.

 Medical Center | K-307 (306408)

Mike O’Reilly, PhD - Professor, Department of Pediatrics - Neonatology

Zoom: https://rochester.zoom.us/j/97634917477?pwd=bjVvblg4RUoyY2o3MmFMTTVDQWE5QT09
Meeting ID: 976 3491 7477
Passcode: 664735

Breakfast Items & Coffee available at 8:30 am in KMRB 3-9623

 Feb 10, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Ian Stone - Graduate Student, Advisor: Andrew Samuelson, PhD

Aging leads to the steady decline in a variety of factors associated with cellular health, resulting in the development of severe age-associated diseases. One such hallmark of aging is dysregulation of the proteome (loss of proteostasis), an important component of neurodegenerative conditions such as Alzheimer’s Disease (AD). SARS-CoV-2 infections have been associated with increased rates of death among AD patients, suggesting an important link between aging and viral infection. Many individual genes have now been identified that are able to singly affect lifespan by altering their activation levels. We hypothesized that genetic perturbations that extended longevity and preserved proteostasis would correlate with viral protection. To test this hypothesis, we approached it from the contrasting perspectives of mutations that extended longevity (increased lifespan) and the reverse, progeria (decreased lifespan). Caenorhabditis elegans (C. elegans) remains a powerful genetic model system for studying aging. Our laboratory uses two primary methods for assessing aging in C. elegans: longevity (knocking out a gene to increase lifespan) and progeria (knocking out a gene to reduce lifespan). We screened longevity mutants for viral resistance using a natural viral pathogen, Orsay virus (OV). We discovered that those with inactivated target of rapamycin (mTOR) complexes had a lower OV load and decreased activation of the intracellular pathogen response (IPR) pathway, suggesting that that these animals have enhanced viral resistance. Previous research from our laboratory identified a group of genes which, when inactivated, resulted in progeria in C. elegans. I tested this panel and found a subset that had reduced expression of the IPR during OV infection. These virally susceptible progeric (Visser) genes were tested for changes in viral pathogenicity using a reporter strain for intestinal shape; several genes were found to be important for viral protection as their inactivation resulted in intestinal bloating. Through dissecting both directions of aging and their relationship to viral immunity, our results have indicated that the longevity mutant mTOR has enhanced viral resistance, whereas some of the progeric mutants are more susceptible to viral infection. These findings suggest a potential inverse correlation for the role of genes in longevity and viral innate immunity. Through continuing our study of the temporal and tissue-specific requirements for mTOR pathway components, we will be able to identify necessary genes involved in connections between viral innate immunity and longevity mechanisms.

 Feb 09, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Ke Du PhD - Assistant Professor of Chemical/Environmental Engineering, UC Riverside (Formerly RIT)

 Feb 08, 2023 @ 3:30 p.m.

 Kornberg Medical Research Building | 3.9624

Jordana Schmierer - Graduate Student, Advisor: Toru Takimoto, DVM, PhD

Pandemic Influenza A viruses (IAVs) have emerged due to genetic reassortment between human and avian or swine IAVs. Host adaptative mutations, particularly in the viral RNA-dependent RNA-polymerase (vRdRp), are required for productive infection and replication in mammals. Pandemic 2009 H1N1 (pH1N1) virus is a reassortant virus with two polymerase components, PA and PB2, originating from avian IAV, which typically does not function well in mammalian cells. Our previous research revealed that mutations in PA played a major role in mammalian host adaptation of pH1N1 and we have identified key mutations in both the N-terminal and C-terminal domains (CTD). However, the mechanisms of polymerase activation through these PA mutations are currently not known. The PA CTD is involved in interactions with viral nucleocapsid protein and host RNA polymerase II, and importantly, plays a key role in polymerase oligomer formation, essential for viral genome replication. We hypothesize that adaptive mutations in the PA CTD regulate viral genome replication kinetics. To test the effect of PA mutations in genome replication, we modified and optimized the Luciferase reporter gene assay to measure genome replication from a vRNA template to cRNA and vice versa. We characterized genome replication activity using polymerase complexes from pH1N1 virus isolated in 2009 with PA mutants containing key residues from either avian IAV (336L/356K) or from pH1N1 isolated in 2017 (321K/330V). We found that avian virus PA residues attenuated genome replication, while newly acquired mutations in the 2017 pH1N1 PA CTD led to increased genome replication. Furthermore, we rescued 2009 pH1N1 viruses with the PA CTD mutations and tested their effect on virus growth. As expected, the virus with avian PA residues attenuated genome replication and multi-step growth in cultured cells. Together, these data suggest that host adaptive mutations in PA CTD effect genome replication activity of the IAV polymerase. 

 Feb 02, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Jacques Robert, PhD - Professor, Department of Microbiology & Immunology

 Jan 27, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Adam Geber - Graduate Student, Advisor: David Topham, PhD

The immune system is classically divided into two categories: innate and adaptive, where the former responds rapidly and nonspecifically and the latter does so more slowly, precisely, and with greater speed and specificity over time. These conceptual distinctions are most appropriate for adult humans, who have a substantial repertoire of mature naïve lymphocytes that can establish immunological memory to protect against reinfection. Because the infant immune system continues to develop after birth and does not yet have an archive of memory cells, it must be capable of rapid and often nonspecific responses to signals of danger and damage. T cells are crucial to proper functioning of the adaptive immune system and are responsible for recruiting and coordinating immune cells, shaping future responses, and directly killing infected or cancerous cells. CD8+ T cells are canonically known for their cytolytic functions but can also produce cytokines under certain inflammatory conditions. During the last two decades an array of lymphoid immune cells have been described as having innate-type functions and/or a strongly restricted capacity for recognizing foreign antigens. More recently, we have found evidence for a subset of CD8+ T cells that arise in utero during the second trimester, persist variably into adulthood, and behave in an innate-like manner. This project aims to understand the stability of this cellular population, how it is activated, and how it might behave during in vivo infection. We plan to use flow cytometry to distinguish the phenotype of putative fetal innate-like CD8+ T cells (FITs) and single cell RNA-sequencing to compare their transcriptional repertoire to established profiles for conventional CD8+ T cells and other innate-type lymphoid cells. We also intend to use clinical samples collected at birth and in early childhood from a cohort with known respiratory infectious exposures to understand the ways that FITs might respond in vivo to coronaviruses (i.e. OC43, SARS-CoV-2). Our findings might help explain children’s lower COVID-19 disease severity and increased prevalence of post-infectious inflammatory conditions. Ultimately, FITs may serve as an immunomodulatory target for limiting immunopathology and enhancing vaccine efficacy in the vulnerable window of early life.

 Jan 26, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Steve Gill, PhD - Professor, Center for Vaccine Biology & Immunology

 Jan 20, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Ankit Dahal - Graduate Student, Advisor: Minsoo Kim, PhD

Pancreatic cancer is one of the deadliest malignancies with an average five-year survival of mere 2-9%. Emerging evidence suggests that the presence of polymorphonuclear (PMN) myeloid derived suppressor cells (MDSCs) with neutrophil-like phenotypes and morphologies play a major role in adverse clinical outcomes due in part to their contribution in establishing immunosuppressive tumor microenvironment (TME). Despite recent advances in our understanding of MDSC phenotypes and characteristics in the TME, the underlying molecular mechanisms by which classical neutrophils differentiate into MDSC within the TME remails largely unknown.

To investigate the microenvironmental cues that regulate PMN-MDSC differentiation at the tumor site, we established several in vitro co-culture systems using pancreatic cancer cells and 3D spheroid conditions. With live cell migration microscopy, we first showed that neutrophils actively swarmed into the pancreatic cancer spheroids and stayed active for an extended time period in the tumor. We further found that cancer cell culture supernatant significantly extended neutrophil survival and successfully differentiated neutrophils into MDSCs that exhibited decreased type 1 Interferon levels, increased arginase and ROS expression, and had the ability to suppress CD8 cytotoxicity. Additionally, when compared to other forms of neutrophil activators such as LPS and TNF, only tumor conditioned media enhanced neutrophil survival and MDSC differentiation. Our data suggest the presence of novel molecular processes that support MDSC differentiation at the tumor site. To identify the molecular regulators of MDSC formation, we have developed a CRISPR-Cas9 pooled library screen using the immortalized granulocyte-monocyte progenitor cell line, HoxB8. This study will further our understanding of MDSC differentiation and may help to develop therapeutics to limit MDSC development in the TME of pancreatic and other solid cancers.

 Jan 19, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Minsoo Kim, PhD - Professor, Center for Vaccine Biology & Immunology

 Jan 13, 2023 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Andy Phan - Graduate Student, Advisor: Yiping Zhu, PhD

Human immunodeficiency virus 1 (HIV-1) is a pathogen responsible for an ongoing global epidemic, for which there is no curative therapy or protective vaccine. Although there exists antiretroviral therapy (ART) which is effective in suppressing further HIV-1 replication, the virus cannot be eliminated from the patient, and cessation of ART would lead to rebound of viral replication. The major obstacle towards an HIV-1 cure is the persistence of replication-competent viral DNA. In infected cells, latent HIV-1 DNA is transcriptionally silenced and not susceptible to the host immune system or antiretroviral drugs. Latency is commonly associated with the deposition of repressive epigenetic modifications and removal of active epigenetic modifications, which occurs through interactions with cellular proteins, but the exact mechanisms for silencing of viral DNA are not well understood.

By employing a CRISPR-Cas9 knockout screen, we assessed host factors to determine their potential in the silencing of viral gene expression, and identified the cohesin complex subunits SMC1A, SMC3, and RAD21 as cellular proteins responsible for silencing of HIV-1 DNA. We show that depletion of these host factors leads to a significant increase in viral DNA expression. We also assess the ability of Vpr, an HIV-1 accessory protein linked to enhancing viral gene expression, to counteract host-mediated silencing. Our current experiments explore the mechanisms by which the cohesin complex may promote condensation of viral chromatin and therefore contribute to decreased viral gene expression, and the ability of HIV-1 to antagonize this silencing. Expansion in this area of HIV-1 research will contribute to the progress of novel therapies to fully eliminate latent DNA in infected cells.

 Jan 12, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Michael M. Lutz - PhD Candidate, Advisor: Toru Takimoto, DVM,PhD

 Jan 11, 2023 @ 10:00 a.m.

Yuexuan Chen - Graduate Student, Advisor: Ruth Serra-Moreno, PhD

Three years into the COVID-19 pandemic and SARS-CoV-2 remains a biological threat due to the emergence of variants with increased transmissibility, more severe disease and/or better escape from neutralizing antibodies – which might render previous COVID-19 vaccines inefficient. Therefore, there is a need to develop antivirals to treat COVID-19. To reach this goal, a better understanding of the cellular factors essential for SARS-CoV-2 propagation can help identify targets for therapeutic intervention.

Here, we investigated the mechanism by which SARS-CoV-2 generates replication organelles (ROs). ROs are intracellular, membranous structures generated during the replication of all positive-sense RNA viruses. They provide a platform that allows the assembly of the virus polymerase for the successful replication and transcription of the viral genome, and as such, ROs are critical for virus replication. Previous studies reported that coronaviruses use the autophagy machinery to build their ROs, but recent findings have questioned this notion. Our work confirms that autophagy is dispensable to build ROs. Specifically, SARS-CoV-2 uses the non-structural protein NSP6 to recruit early endosomes for RO biogenesis in a clathrin- and COP-I-dependent manner, and that the virus also needs lipid droplets and mitochondria to meet its lipid demands for this massive membrane rewiring.

 Jan 05, 2023 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Sebastian Bosch - Graduate Student, Advisor: Stephen Dewhurst, PhD

Despite the transformation of HIV-1 infection into a chronic but manageable condition through combination anti-retroviral therapy (cART), HIV-associated neurocognitive disorders (HAND) continue to affect as many as 45% of persons living with HIV. Microglia are the main cell type that HIV productively infects within the central nervous system (CNS) and in pathologic settings such as HAND, can contribute to neuroinflammation and tissue damage. One way that microglia communicate with other cell types is through the secretion of exosomes, which can transfer nucleic acids, proteins and additional biological mediators to other CNS cell types. HIV infection alters the content of these exosomes, including their mRNA and microRNA (miRNA) cargo, and we hypothesize that this may contribute to synaptodendritic damage in recipient neurons. Altered exosome content in the context of HIV-1 infection may additionally contribute to reactivation of bystander microglial cells. Microglia become reactivated upon infection by HIV-1, resulting in morphological changes, secretion of pro-inflammatory cytokines and chemokines, and an increase in synaptic pruning activity, which collectively contribute to neurocognitive decline associated with HAND. Most previous studies to assess the contents of microglial exosomes have taken a highly reductionist approach, in which microglia have been exposed to a single HIV-1 protein, such as Tat or Nef. To address this, we have begun to develop both in vitro and in vivo models for HIV infection of human microglia. As a first step, we have induced the differentiation of cultured WA09 human embryonic stem cells (ESCs) towards CD43+/CD235a+ human pluripotent stem cells (HPSCs). We have then either: (A) engrafted the HPSCs into Rag2/IL2r x human mCSF knockin mice for development of a humanized microglial mouse model or (B) further differentiated the HPSC in vitro, towards CD45/CD11b+ human microglia. In parallel, we are also developing methods for exosomes from cultured microglia. We have successfully isolated exosome-like particles from HIVNanoLuc CHME5 cells, a microglial cell line containing an integrated HIV-1 YU2 provirus expressing NanoLuciferase (that enables simple monitoring of proviral activation following TNF-α treatment). Exosome like-particles were examined by nanoparticle tracking analysis to determine their size and density; these studies confirmed the presence of particles with the size distribution (30-150nm) of canonical exosomes. Furthermore, we showed these exosome-like particles contained the tetraspanins CD63 and CD9, further supporting their identity as microglia derived exosomes. Ultimately, our goal is to use our in vitro and in vivo experimental models for HIV infection of human microglia, to characterize HIV-induced changes in the RNA content of microglial exosomes, and their biological/functional effects on exposed but uninfected “bystander” microglia and neurons.

 Dec 15, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Steve Gill, PhD - Professor, Department of Microbiology & Immunology

 Dec 09, 2022 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Justin Brennan - Graduate Student, Advisor: Yan Sun, PhD

Defective viral genomes (DVGs) are truncated derivatives of their parental viral genomes unable to replicate in the absence of a full-length helper virus. DVGs have been observed in most RNA viruses and play critical roles in viral pathogenesis and viral evolution. Specifically, the copy-back type of DVGs (cbDVGs) are potent inducers of the antiviral response during Mononegavirales infection including respiratory syncytial virus (RSV) infection. RSV is among the most consequential causative agents of severe pediatric respiratory illness worldwide and RSV cbDVGs in pediatric patients correlate with enhanced antiviral responses; thus cbDVGs are potential candidates for antivirals and vaccine adjuvants. Currently, little is known about the mechanisms governing cbDVG generation or species-specific functions of cbDVGs, limiting our ability to utilize cbDVGs to mitigate pathology caused by viral infections. Our lab has previously shown that RSV cbDVG generation is not a stochastic process and identified three genomic “hotspots” (R1, R2 and R3) mediating the formation of cbDVGs. Moreover, the introduction of an 8U mutation into R1 was observed to reduce its role in cbDVG formation during infection. Here, I expanded on these studies by generating a mutant virus with a similar mutation in R2 (R2-8U). WT and R2-8U cbDVGs were enriched by high MOI passaging. Strikingly, RNA-seq analysis of DVG enriched virus stocks (HD) showed that the frequency of R2 cbDVGs produced by R2-8U was largely reduced, while R2 cbDVGs dominated WT HD. Unexpectedly, R2-8U HD contained a 1.5 log increase in total cbDVG reads and frequency relative to WT HD. To test how these large differences in cbDVG composition and total amount affect viral infection and antiviral responses, A549 cells were infected with WT HD (enriched with R2 cbDVGs) and R2-8U HD (enriched with R3 cbDVGs) at the same MOI. Interestingly, WT HD and R2-8U HD induced similar expression levels of IFNB1, IFNL1 and ISGs despite a greater abundance of cbDVGs contained in R2-8U HD than WT HD, suggesting that R2 cbDVGs more efficiently induce the interferon response than R3 cbDVGs. Additionally, qPCR targeting specific cbDVG species indicated that R3 cbDVGs replicate faster than R2 cbDVGs. Taken together, these data further support our lab’s previous findings that cbDVG generation is genetically manipulable and provide evidence for the broader hypothesis in the Mononegavirales field that different cbDVGs have distinct functions.

 Dec 08, 2022 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Megan L. Falsetta (Wood), PhD - Assistant Professor, Obstetrics and Gynecology

 Dec 05, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Joshua Munger, PhD - Professor, Departments of Biochemistry & Biophysics and Microbiology & Immunology

 Dec 02, 2022 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Mukta Palshikar - PhD Candidate, Advisor: Juilee Thakar, PhD

 Dec 01, 2022 @ 1:00 p.m.

 Medical Center | K-207 (2-6408)

Darline Castro-Melendez - Graduate Student, Advisors: Kristin Scheible, MD, Paige Lawrence, PhD

Per- and polyfluoroalkyl substances (PFAS) are persistent synthetic chemicals widely used in industrial processes and consumer goods, and they are ubiquitous in the environment and people. Epidemiological studies have associated exposure to PFAS with detrimental effects on the immune system, and fetuses and infants are particularly susceptible to environmental exposures due to their rapid growth and developing systems. During fetal development, each immune cell type develops at different gestational stages, thus perturbations during pregnancy could alter the normal establishment of these immune layers. There is strong evidence of PFAS-associated immunotoxicity and its effects on vaccine responses; however little attention has been drawn to how these compounds affect early life T cell development. Here we hypothesize that maternal PFAS exposure during pregnancy disrupts infant T cell development in humans. In our cohort of 199 human subjects, our preliminary data suggest a modulation of the IL-21 producing CD4+ population, a cell type that supports antibody maturation, revealing a possible link to suppressed antibody responses associated with PFAS. Using a systems immunology approach, we show the phenotypic and time-dependent complexity within the CD4+ T cell pool at birth, six and twelve months of age through high-dimensional single-cell analysis. We further identify specific immune population clusters associated with PFAS exposure during pregnancy; our data gives us further insight into the complexity of the immune response during infancy and the impact of antenatal exposures on reshaping the fetal developmental program.

 Dec 01, 2022 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Ma Rie Kim - PhD Candidate, Supervised by Dr. Minsoo Kim

Zoom Passcode:  000412

Abstract: Neutrophils have traditionally been defined as terminally differentiated innate immune cells with homogeneous phenotypes and antimicrobial functions. However, growing evidence highlights the previously underappreciated diversity and heterogeneity of this cell type. Rather than mere changes in number or morphology, neutrophils have been demonstrated to have transcriptional plasticity, mainly studied in context of the tumor microenvironment or chronic inflammations. Whether neutrophil heterogeneity affects functional adaptations to acute infections or in severe inflammation remains largely unknown. Furthermore, it is yet unknown what homeostatic factors induce neutrophil heterogeneity and the implications of the resulting phenotypic and functional diversity on the host response to inflammation and infection.

Here, we demonstrate that neutrophils are primed by microbiome-derived factors in the blood at homeostasis that leads to anti-inflammatory transcriptional changes. We show that this homeostatic priming is variable among individuals and that this heterogeneity is reflected in the phenotypes and functions of neutrophils in response to inflammatory stimuli. Using mouse models, we demonstrate that increased microbiome exposure via gut-derived extracellular vesicles (EVs) leads to favorable outcomes to systemic inflammation, such as sepsis. Collectively, our data suggest that functional heterogeneity of neutrophils is primed by microbiome-derived factors at homeostasis, leading to altered host response to subsequent infection.

 Dec 01, 2022 @ 11:00 a.m.

Terry Wright, PhD - Professor, Departments of Pediatrics and Microbiology & Immunology

 Nov 18, 2022 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

David J. Barnard - PhD Candidate, Advisor: Martin Pavelka, PhD

 Nov 17, 2022 @ 1:00 p.m.

 Medical Center | K-207 (2-6408)

Kala Hardy - Graduate Student, Advisor: Toru Takimoto, PhD

Many viruses evade the host innate immune response to replicate efficiently within the host. In the case of SARS-CoV-2, nonstructural protein 1 (nsp1) is known to play a major role in immune evasion by inducing general shutoff of host protein translation. Its C-terminal domain binds to the mRNA entry site in ribosomes, thus inhibiting host protein synthesis and expression of antiviral proteins. Nsp1 is expressed by all human coronaviruses (CoVs), but its functions and strategy to induce host shutoff are not fully understood. Nsp1 of human alpha-CoV (α-CoV) NL63 and 229E lacks the C-terminal domain known to be essential for the shutoff activity of SARS-CoV-2 nsp1. However, I found that the shutoff activity of α-CoV NL63 was much greater than that of SARS-CoV-2, suggesting that it induces general shutoff by a different unrecognized mechanism(s). I found that, in contrast to nsp1 from SARS-CoV-2, NL63 nsp1 localized in the nucleus and significantly decreased the amount of reporter gene mRNA in whole cell lysates. To determine how it is affecting mRNA, I labeled newly synthesized mRNAs in nsp1-expressing cells and found that NL63 nsp1 prevented de novo RNA synthesis. Strikingly, in cells transfected with NL63 nsp1 as well as in NL63-infected cells, Rpb1 (the catalytic subunit of RNA Polymerase II) disappeared, suggesting that NL63 nsp1 may initiate Rpb1 degradation via the cell’s “last resort” pathway to clear stalled RNA Pol II. This does not appear to be a conserved mechanism among α-CoV nsp1s, as 229E nsp1 has much weaker shutoff activity and does not affect reporter gene mRNA levels. To further elucidate the mechanism of nsp1-induced shutoff, I constructed a series of chimeric α-CoV nsp1s to identify the key domain(s) involved in shutoff activities, and I plan to rescue NL63 viruses containing these chimeras. This research will investigate the impact of nsp1-mediated shutoff on host innate responses to infection as well as the mechanism of Rpb1 degradation by NL63 nsp1.

 Nov 17, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Elsa Bou Ghanem, PhD - Assistant Professor, Department of Microbiology and Immunology, University at Buffalo

Streptococcus pneumoniae (pneumococcus) remain the leading cause of community-acquired pneumonia in the elderly. Our work aims to understand the age-driven changes in neutrophil responses against these bacteria and the underlying pathways driving immune-senescence for improved therapeutic/preventative options. Th seminar will focus on 1) how neutrophil responses are altered with age, 2) the role of ROS production by the mitochondria in antibacterial function of these innate immune cells, and 3) how these responses are controlled by extracellular adenosine signaling.

 Nov 14, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Steven Gill, PhD

Mark Sangster, PhD - Professor, Center for Vaccine Biology and Immunology

 Nov 11, 2022 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Chantelle Lehone White - Graduate Student, Advisor: Andrea Sant, PhD

Although there has been much research into immunity generated by SARS-CoV-2 infection, there is little known about cellular immunity to endemic, seasonal human coronaviruses (sHCoVs). Understanding CD4 T cell memory generated by intermittent sHCoV infections is important as it may reveal whether α-sHCoVs and β-sHCoVs, which utilize distinct receptors and potentially alternative tropisms, induce similar immunity. Additionally, cross-reactive memory generated by sHCoV infections may be recalled upon exposure to SARS-CoV-2, impacting vaccination and infection outcomes. To evaluate these issues, CD4 T cells isolated from PBMCs collected prior to 2020 were stimulated with peptides representing the translated region of the Spike (S), S1 and S2 domains or Nucleocapsid (N) proteins from each sHCoV as well as influenza proteins as a comparator. The magnitude and functional potential of CD4 T cells were quantified by EliSpot assays and multiparameter flow cytometry. These studies revealed that the magnitude and specificity of CD4 T cell responses to sHCoV S and N varied across individuals, with a significant age-associated decline in the response magnitude. There was a notable bias towards the S2 domain, highlighting the impact of repeated exposures to conserved sHCoV epitopes and potential to be called into SARS-CoV-2 responses. CD4 T cells elicited by each virus demonstrate distinct functional potential, particularly NL63 and HKU1-reactive CD4 T cells that exhibit robust cytotoxic potential. These studies reveal the age and strain specific variability in both the magnitude and functionality of sHCoV-reactive CD4 T cells across individuals. Such variability could reveal the cellular consequences associated with periodic encounters with sHCoV as well as the potential impact of these memory responses on subsequent SARS-CoV-2 infections.

 Nov 10, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Lara Abramowitz, PhD - Staff Scientist, Laboratory of Cell and Molecular Biology, NIDDK/NIH

 Nov 07, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Jacques Robert, PhD

Matthieu Paiola, PhD - Postdoctoral Fellow, Robert Lab, Department of Microbiology & Immunology

 Nov 04, 2022 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Michael Sportiello - Graduate Student, Advisor: David Topham, PhD

After an acute respiratory infection is cleared, most T cells that controlled the infection die off. Tissue resident memory CD8 T cells (TRM) remain in the lung, poised to fight off a recurrent infection. As demonstrated in mouse models, these TRM have large impacts on the survival and morbidity of repeated infection. While many have studied this subset to understand what causes differentiation into this essential T cell subset, a master regulator of this phenotype remains elusive. To these ends, RNA sequencing and ATAC sequencing experiments of TRM were conducted after viral clearance to investigate the existence of a master regulator. Transcription factor Nfil3 became a likely candidate after integrated omics and differential expression and accessibility analyses. Its downstream targets were also enriched. Flow cytometry to fully characterize the levels of Nfil3 in all T cell subsets of the lung, spleen, and draining lymph node was conducted 2, 7, 14, and 43 days post infection (dpi). At days 7, and 14 dpi, Nfil3 correlated with pre-TRM markers. At 43 dpi, Nfil3 was highest in TRM and lowest in central memory T cells. Finally, experiments were performed to investigate if Nfil3 played a causal role in TRM development or maintenance. Lentivirus constructs to over- or under-express Nfil3 were then created to transduce T cells, and an inducible mouse model was created to flox out Nfil3 at different points during and after infection. Preliminary results paint a picture of Nfil3 playing an important role in the differentiation of T cells post infection, and future work should move to human cells to investigate Nfil3 in humans.

 Nov 03, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Gowri Muthukrishnan, PhD - Assistant Professor, Center for Musculoskeletal Research, Department of Orthopedics

 Oct 31, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Scott Gerber, PhD - Professor, Departments of Surgery and Microbiology & Immunology

 Oct 28, 2022 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

Tara Vrooman - Graduate Student, Advisor: Scott Gerber, PhD

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy that is currently the fourth leading cause of cancer related deaths, with a 5-year survival rate of only 10%. Surgical resection is the only successful cure thus far, but even with resection there is an 80% chance of recurrence. Immunotherapy, which involves stimulating the immune system to recognize and destroy tumor cells, has emerged as a viable therapy for a variety of tumors, but has been largely unsuccessful in treating PDAC due to the inherent suppressive nature of this malignancy. However, recent data suggests that the efficacy of immunotherapy may be enhanced when combined with standard of care treatments such as radiotherapy. Our laboratory has developed a novel treatment that combines the potent antitumor immune cytokine, interleukin-12 (IL-12) with highly effectivestereotactic body radiation therapy (SBRT), which results in remarkable tumor control and cure in a preclinical orthotopic model of PDAC.

Due to the high likelihood of recurrence in this malignancy, we investigated whether this combinatorial treatment approach can promote long-lasting antitumor immunity. Our data demonstrated that mice cured of primary PDAC tumors following SBRT + IL-12 therapy are protected against tumor rechallenge for as long as 8 months post-cure. Importantly, transfer studies revealed that CD4+ memory T cells, but not CD8+ memory T cells are the predominant immune subset responsible for long-lasting immunity. We further characterized this CD4+ T cell memory subset and determined that the cells within the peripheral lymphoid tissues expressed phenotypic markers for central memory T cells (Tcm), which have been reported to be ideal for providing durable antitumor immunity. Additionally, while investigating the cured pancreas 6-8 months after treatment, we observed pronounced changes in tissue architecture by immunohistochemistry and flow cytometry, with adipose rich areas containing abundant CD4+ T cells, which exhibited a tissue-resident memory (Trm) phenotype of CD44+, CD62L-, & CD69+. These data suggest that local SBRT + IL-12 therapy results in the presence of long-lived Trm cells in the pancreas that may be poised to attack recurrent tumor cells.Future plans will translate these findings into a clinical trial where PDAC patients eligible for surgical resection will first receive treatment with SBRT + IL-12 in a neoadjuvant setting before surgery. We hypothesize this innovative combination therapy will act as an in-situ vaccine and induce memory cells toprotect against PDAC recurrence

 Oct 27, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6804)

Alessandro Venosa, PhD - Assistant Professor, University of Utah

EHSC Seminar Series Highlighted Topic: Air Pollution and Pulmonary Toxicity

 Oct 27, 2022 @ 11:00 a.m.

 Medical Center | 4-8820

Sydney Simpson, PhD - Senior Scientist Research & Development, Ortho Clinical Diagnostics

In early 2020 SARS-CoV-2 rapidly spread across the globe and was declared a pandemic in mid-March 2020. Less than one month later Ortho Clinical Diagnostics, an in vitro medical diagnostic device manufacturer, released the first high-throughput SARS-CoV-2 antibody assay to aid in diagnosis of infection and allow for early monitoring of the spread of the virus across the US. Ortho released another four SARS-CoV-2 assays world-wide within the next year to continue in the battle to understand and control COVID-19. Ortho Clinical Diagnostics rapid response to the Covid-19 pandemic illustrates the positive impact scientists in industry can have on society and support evolving government guidance and policies. Several in vitro diagnostics assays developed during a world-wide pandemic, their uses and implications, and their positive role in managing the Covid-19 public health crisis will be discussed.

 Oct 24, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Andrea Sant, PhD - Professor, Center for Vaccine Biology & Immunology

 Oct 21, 2022 @ 9:00 a.m.

 Medical Center | K-207 (2-6408)

Yuhang Shi - Graduate Student, Advisor: Ruth Serra-Moreno, PhD

 Oct 20, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Edward Schwarz, PhD - Professor, Center for Musculoskeletal Research

 Oct 14, 2022 @ 9:00 a.m.

 Medical Center | k-207 (2-6408)

Edward Schwarz, PhD - Professor, Departments of Orthopedics and Microbiology & Immunology

 Oct 14, 2022 @ 9:00 a.m.

 Kornberg Medical Research Building | 3-9624

John Miller - Graduate Student, Advisors: Rachael Turner, M., PhD and Minsoo Kim, PhD

 Oct 13, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Zirui Zhou - MBI Student, Advisor: Michelle Dziejman, PhD

 Sep 15, 2022 @ 12:30 p.m.

 Medical Center | k-307 (3-6408)

Shelby Peres - MBI Student, Advisor: Martin Pavelka, PhD

 Sep 15, 2022 @ 12:00 p.m.

 Medical Center | K=307 (3-6408)

Robin Stephens, PHD, MA - Associate Professor and Director, Neuroinflammation Department of Pharmacology, Physiology and Neuroscience Rutgers, New Jersey Medical School

Persistent infection generates Th1/Tfh Hybrid effector T cells and effector memory T cells (Teff, Tem) in the long term, and both contribute to protection in Plasmodium infection. While specific antibody levels remain stable after the acute phase of P. chabaudi infection, the decay of T cells corresponds with loss of protection from re-infection. We tested chronic vaccine vector MCMV to prolong protection. Boosting live malaria vaccine with MCMV-B5: i) prolonged vaccine protection to heterologous infection at day 200, ii) increased parasite-specific T cells and promoted a highly-differentiated Teff phenotype. Importantly, chronic MCMV infection itself improved protection from P. chabaudi infection and promoted maintenance of pre-activated CD8a+ dendritic cells through IFN-g. Our findings suggest a mechanism to boost CD4 T cell immunity using chronic vaccines, which may be broadly applicable to infections that require T cell-based immunity.

 Sep 12, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Felix Yarovinsky, MD

Sara Ahmed; Tyrus Perdue - PhD Candidate, Advisor: Felix Yarovinsky, MD; PhD Candidate, Advisor: Cynthia Monaco, MD, PhD

 Sep 01, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Cassandra Houser - PhD Candidate in Microbiology & Immunology

 Jul 18, 2022 @ 12:00 p.m.

 Medical Center | Ryan Case Method Room 1-9576

Host: Dr. Paige Lawrence, Microbiology & Immunology Program, University of Rochester School of Medicine & Dentistry

Katharine F. Tomberlin - PhD Candidate, Advisor: Michelle Dziejman, PhD

 Jun 28, 2022 @ 1:00 p.m.

 Medical Center | Ryan Case Method Rm (1-9576)

Sean A. Nelson - PhD Candidate, Advisor: Andrea Sant, PhD

 Jun 23, 2022 @ 9:00 a.m.

 Medical Center | Adolph Aud. (1-7619)

Host: Microbiology & Immunology

Taylor Uccello - PhD Candidate in Microbiology & Immunology

https://urmc.zoom.us/j/96694259171?pwd=ZGJTWlNpQmFaZVBWamRNZDdVN0tIZz09 Passcode: 168998

 Jun 03, 2022 @ 1:00 p.m.

 Medical Center | Adolph Auditorium 1-7619

Host: Dr. Scott Gerber, Microbiology & Immunology Program

Katharine Tomberlin - PhD Candidate, Advisor: Michelle Dziejman, Ph.D.

 May 26, 2022 @ 12:00 p.m.

Zanah Francis - PhD Candidate, Advisor: Marty Pavelka, Ph.D.

 May 19, 2022 @ 12:00 p.m.

Peter Walter, PhD - SVP & Institute Director, Altos Labs - Bay Area Institute of Science
Distinguished Professor Emeritus
University of California, San Francisco
Department of Biochemistry & Biophysics

 May 16, 2022 @ 9:30 a.m.

 Medical Center | Class of '62 Auditorium and Atrium

Host: Genetics Day is sponsored by the University Committee for Interdisciplinary Studies (UCIS) and organized by the Departments of Biomedical Genetics and Biology

Mary Kate Moran - PhD Candidate, Advisors: Lisa Beck, M.D. and Steven Gill, Ph.D.

 May 12, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Zhenqiang Yao, PhD - Associate Professor, University of Rochester
Pathology & Laboratory Medicine

 May 09, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Microbiology and Immunology Department Seminar Series: Joint Faculty Candidate

Hannah Bell - PhD Candidate, Advisor: Michelle Dziejman, PhD

 May 09, 2022 @ 9:30 a.m.

Host: Microbiology & Immunology Ph.D. Thesis Seminar

Andrew Martin - PhD Candidate, Advisor: Felix Yarovinsky, M.D.

 May 05, 2022 @ 12:00 p.m.

Lisa Beck, MD - Professor, Dermatology

 Apr 29, 2022 @ 8:30 a.m.

Host: CVBI

Michael Lutz - PhD Candidate, Advisor: Toru Takimoto, D.V.M., Ph.D.

 Apr 28, 2022 @ 12:00 p.m.

Sydney Simpson, PhD - Senior Scientist, Ortho Clinical Diagnostics

 Apr 25, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Ruth Serra-Moreno, PhD and Microbiology and Immunology Department Seminar Series

Scott Gerber, PhD - Associate Professor, Surgery / Microbiology and Immunology/Radiation Oncology

 Apr 22, 2022 @ 8:30 a.m.

 Medical Center | Lower Adolph Auditorium (1-7619)

Host: CVBI

Aizan Embong - PhD Candidate, Advisor: David Topham, Ph.D.

 Apr 21, 2022 @ 12:00 p.m.

Josh Munger, PhD - Professor, Biochemistry & Biophysics, Univ. Rochester

 Apr 20, 2022 @ 3:30 p.m.

 Kornberg Medical Research Building | 3.9624

Leigh Knodler, PhD - Associate Professor, Paul G. Allen School for Global Health
College of Veterinary Medicine
Washington State University

 Apr 18, 2022 @ 12:00 p.m.

 Medical Center | K-207 (2-6408)

Host: Microbiology and Immunology Department Seminar Series: Special Faculty Candidate Seminar

Kristin Scheible, MD - Professor, Pediatrics / Microbiology and Immunology

 Apr 15, 2022 @ 8:30 a.m.

 Medical Center | Lower Adolph Auditorium (1-7619)

Host: CVBI

Ashwin B.R. Kumar - PhD candidate in BioPhysics, Advisor: David Topham, PhD

 Apr 14, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Microbiology and Immunology Student Seminar

Ashwin Kumar - PhD Candidate, Advisor: David Topham, Ph.D.

 Apr 14, 2022 @ 12:00 p.m.

Katrina Korfmacher, PhD - Professor, Environmental Medicine, Univ. Rochester

 Apr 13, 2022 @ 3:30 p.m.

Sergio M. Pontejo, PhD - Research Fellow, Laboratory of Molecular Immunology
National Institute of Allery & Infectious Diseases (NIAID)

 Apr 12, 2022 @ 4:00 p.m.

 Medical Center | Ryan Case Method Room (1-9576)

Host: David H. Smith Center for Vaccine Biology: Faculty Candidate Seminar

Henri Tiedge, PhD - Distinguished Professor, Physiology and Pharmacology, Neurology, Medicine
Downstate Health Sciences University

 Apr 11, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7618)

Host: Microbiology and Immunology Department Seminar Series

Ya-Chi Ho, MD, PhD - Assoc. Professor, Infectious Disease & Microbial Pathogenesis - Yale University

 Apr 08, 2022 @ 11:00 a.m.

 Medical Center | Class of '62 Auditorium

Host: Medical Scientist Research Symposium

Felix Yarovinsky, PhD - Professor, Microbiology and Immunology, CVBI

 Apr 08, 2022 @ 8:30 a.m.

 Medical Center | Lower Adolph Auditorium (1-7619)

Host: CVBI

Christie Gilbert - PhD Candidate, Advisor: Steven Gill, Ph.D.

 Apr 07, 2022 @ 12:00 p.m.

Regina Rowe, MD - Professor, Pediatrics, Univ. Rochester

 Apr 06, 2022 @ 3:30 p.m.

 Kornberg Medical Research Building | 3.9624

Margaret Schwarz, MD - Professor, Pediatrics Indiana University School of Medicine

 Apr 05, 2022 @ 12:00 p.m.

 Medical Center | Lower Adolph Auditorium (1-7619)

Sheyda Azimi, PhD - Cystic Fibrosis Foundation Postdoctoral Fellow, Georgia Institute of Technology

 Apr 04, 2022 @ 12:00 p.m.

 Medical Center | K-207 (2-6408)

Host: Microbiology and Immunology Department Seminar Series: Faculty Candidate

Jared Benjamin - MS Candidate, Advisor: Ruth Serra-Moreno, PhD

 Apr 04, 2022 @ 10:00 a.m.

 Medical Center | K307 (3-6408)

Bailey Kinn; Clare Heffernan - MS Candidate, Advisor: Paul Dunman, Ph.D.; MS Candidate, Advisors: Charles Chu, Ph.D. and Jacques Robert, Ph.D.

 Mar 31, 2022 @ 12:00 p.m.

James Gurney, PhD - Cystic Fibrosis Postdoctoral Research Fellow, Georgia Institute of Technology

 Mar 31, 2022 @ 10:00 a.m.

 Medical Center | K207 (2-6408)

Host: Dept. of Microbiology & Immunology Seminar Series

Chris Anderson, PhD - Professor, Pediatrics, Univ. Rochester

 Mar 30, 2022 @ 3:30 p.m.

Elizabeth Evans, PhD - Chief Operating Officer Vaccinex, Senior Vice President, Discovery and Translational Medicine

 Mar 28, 2022 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7618)

Host: Ruth Serra-Moreno, PhD & Microbiology and Immunology Department Seminar Series

John DiPersio, MD, PhD - Chief, Division of Oncology
Washington University School of Medicine

 Mar 25, 2022 @ 12:00 p.m.

Host: The Wilmot Cancer Institute Series Inaugural Lowry Seminar

Brian Altman, PhD - Professor, Biomedical Genetics

 Mar 25, 2022 @ 8:30 a.m.

 Medical Center | Adolph (Lower) Auditorium (1-7619)

Host: CVBI

Shuyang Sue Qin - PhD Candidate, Advisors: Peter Prieto, M.D., M.P.H.
Scott Gerber, Ph.D.

 Mar 24, 2022 @ 1:00 p.m.

 Medical Center | Adolph Auditorium (1-7619)

Ian Stone - PhD Candidate, Advisor: Andrew Samuelson, Ph.D.

 Mar 24, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Yan Sun, PhD - Professor, MBI, Univ. Rochester

 Mar 23, 2022 @ 3:30 p.m.

 Kornberg Medical Research Building | 3.9624

Karli M. Norville - PhD Candidate, Advisor: John Frelinger, Ph.D.

 Mar 23, 2022 @ 10:00 a.m.

Jean Celli, PhD - Professor, Paul G. Allen School for Global Health
College of Veterinary Medicine
Washington State University

 Mar 21, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Meera Singh, PhD - Assistant Professor, Department of Neurology: Stroke Division

 Mar 18, 2022 @ 8:30 a.m.

 Medical Center | Upper Auditorium (3-7619)

Host: CVBI

Caroline Junqueira, PhD - Associate Professor, Oswaldo Cruz Foundation
Research Associate, Boston Children’s Hospital
Harvard Medical School

Dr. Junqueira is an Associate Professor at Oswaldo Cruz Foundation (Brazil) and a Research Associate at Boston Children’s Hospital, Harvard Medical School, and an Affiliate Member of the Brazilian Academy of Sciences. Her current research work is focused on effector immunological  mechanisms against intracellular pathogens and cancer, with emphasis on Plasmodium spp infections.

 Mar 17, 2022 @ 4:00 p.m.

 Medical Center | Adolph (Lower) Auditorium (1-7619)

Host: David H. Smith Center for Vaccine Biology & Immunology

Andy Phan; Jordana Schmierer - PhD Candidate, Advisor: Toru Takimoto, D.V.M., Ph.D.; PhD Candidate, Advisor: Yiping Zhu, Ph.D.

 Mar 17, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Andrew Cameron, PhD - Assistant Director, Clinical Microbiology, Univ. Rochester

 Mar 16, 2022 @ 3:30 p.m.

 Kornberg Medical Research Building | 3.9624

Eva Nogales, PhD - Professor; Howard Hughes Medical Institute Investigator, Department of Biochemistry and Molecular Biology, University of California, Berkeley, CA

 Mar 16, 2022 @ 1:00 p.m.

 Medical Center | Class of '62 (G-9425)

Host: Dr. Lynne Maquat, PI, and Dr. Jeffrey Hayes, Co-PI, NIH T32 in Cellular, Biochemical and Molecular Sciences (Co-sponsored by GWIS)

Adam Geber; Ankit Dahal - PhD Candidate, Advisor: David Topham, Ph.D.; PhD Candidate, Advisor: Minsoo Kim, Ph.D.

 Mar 10, 2022 @ 12:00 p.m.

 Medical Center | K-307 ()3-6408)

Ruth Serra-Moreno, PhD - Professor, MBI, Univ. Rochester

 Mar 09, 2022 @ 3:30 p.m.

Nir Drayman, PhD - Postdoctoral Fellow, Dr. Savas Tay Lab, School of Molecular Engineering, University of Chicago

 Mar 08, 2022 @ 4:00 p.m.

 Medical Center | Ryan Case Method Room (1-9576)

Host: David H. Smith Center for Vaccine Biology & Immunology and Department of Microbiology & Immunology

Ralph DeBerardinis, MD, PhD - Chief and Professor, Division of Pediatric Genetics and Metabolism
Children’s Medical Center Research
Institute at UT Southwestern
Howard Hughes Medical Institute (HHMI)

Ralph DeBerardinis earned a B.S. in biology from St. Joseph’s University and M.D. and Ph.D. degrees from the University of Pennsylvania. Dr. DeBerardinis performed postdoctoral research in Craig Thompson’s laboratory in the Penn Cancer Center from 2004 to 2007. Here, he performed seminal work elucidating the importance of metabolism to tumorigenesis. He joined the faculty of the University of Texas Southwestern Medical Center in 2008 and joined the Children’s Medical Center Research Institute at UT Southwestern (CRI) in 2012. He holds the Joel B. Steinberg, M.D. Chair in Pediatrics, and he is a Sowell Family Scholar in Medical Research and a Robert L. Moody Faculty Scholar. Dr. DeBerardinis became a Howard Hughes Medical Institute (HHMI) Investigator in 2018 and was elected to the National Academy of Medicine in 2020. 

 Mar 08, 2022 @ 10:00 a.m.

Host: URMC Metabolism Meeting Special Seminar

Bonnie Bassler, PhD - Howard Hughes Medical Institute Investigator, Squibb Professor and Chair, Department of Molecular Biology, Princeton University

 Mar 07, 2022 @ 12:00 p.m.

Host: Microbiology Graduate Students

Yuexuan Chen - PhD Candidate, Advisor: Ruth Serra-Moreno, Ph.D.

 Mar 03, 2022 @ 12:30 p.m.

Darline Castro-Melendez - PhD Candidate, Advisors: Kristin Scheible, M.D. and Paige Lawrence, Ph.D.

 Mar 03, 2022 @ 12:00 p.m.

Toru Takimoto, PhD - Professor, MBI, Univ. Rochester

 Mar 02, 2022 @ 3:30 p.m.

 Kornberg Medical Research Building | 3.9624

Miles W. Carroll, Ph.D. - Professor, High Consequence Emerging Viruses Group
Wellcome Centre for Human Genetics
Nuffield Department of Medicine
Oxford University

 Feb 28, 2022 @ 12:00 p.m.

Host: Brian Ward, Ph.D.

Clive Zent, M.D. - Professor, Department of Medicine: Hematology & Oncology

 Feb 25, 2022 @ 8:30 a.m.

 Medical Center | Class of '62 Auditorium

Host: CVBI

Justin Brennan - PhD Candidate, Advisor: Yan Sun, Ph.D.

 Feb 24, 2022 @ 12:30 p.m.

 Medical Center | K-307

Sebastian Bosch - PhD Candidate, Advisor: Stephen Dewhurst, Ph.D.

 Feb 24, 2022 @ 12:00 p.m.

 Medical Center | K-307

Erica Sanchez, Ph.D. - Assistant Professor, Department of Biology
San Francisco State University
Faculty Candidate

 Feb 24, 2022 @ 10:00 a.m.

 Medical Center | 

Host: Dept. Microbiology - Flyer

Yiping Zhu, PhD - Professor, MBI, Univ. Rochester

 Feb 23, 2022 @ 3:30 p.m.

Tonya J. Webb, PhD - Associate Professor, ACS-IRG & DICR Program Director
Department of Microbiology & Immunology
Marlene and Stewart Greenebaum Comprehensive Cancer Center
University of Maryland School of Medicine

 Feb 21, 2022 @ 12:00 p.m.

Host: Jacques Robert, Ph.D. and NIH/NIAID Predoctoral Training Program in Immunology - T32AI007285

Chantelle White - PhD Candidate, Advisor: Andrea Sant, Ph.D.

 Feb 17, 2022 @ 12:00 p.m.

Meera Singh, PhD - Professor, Neurology, Univ. Rochester

 Feb 16, 2022 @ 3:30 p.m.

Jacques Robert, PhD - Professor, Microbiology and Immunology

 Feb 11, 2022 @ 8:30 a.m.

 Medical Center | Class of '62 Auditorium (G-9425)

Host: CBVI

Tara Vrooman - PhD Candidate, Advisor: Scott Gerber, Ph.D.

 Feb 10, 2022 @ 12:00 p.m.

 Medical Center | 3-6408 and Zoom

Jacques Robert, PhD - Professor, MBI, Univ. Rochester

 Feb 09, 2022 @ 3:30 p.m.

Sharilyn Almodovar, PhD - Assistant Professor, Texas Tech University Health Sciences Center Department of Immunology and Molecular Microbiology

 Feb 07, 2022 @ 12:00 p.m.

 Medical Center | 3-7619 (Upper Aud.)

Host: Ruth Serra-Moreno, Ph.D.

Michael Sportiello - PhD Candidate, Advisor: David Topham, Ph.D.

 Feb 03, 2022 @ 12:00 p.m.

 Medical Center | K-307 (3-6408) & Zoom

Brian Ward, PhD - Professor, MBI, Univ. Rochester

 Feb 02, 2022 @ 3:30 p.m.

Vera Gorbunova, PhD - Co-Director, Rochester Aging Research Center, Department of Biology

 Jan 28, 2022 @ 8:30 a.m.

Yuhang Shi - PhD Candidate, Advisor: Ruth Serra-Moreno, Ph.D.

 Jan 27, 2022 @ 12:00 p.m.

Xing Qiu, PhD - Professor, Biostats Computational Biology, Univ. Rochester

 Jan 26, 2022 @ 3:30 p.m.

Tyler Scherzi - PhD Candidate, Advisor: Kirsi Jarvinen-Seppo, M.D., Ph.D.

 Jan 20, 2022 @ 12:00 p.m.

Jack Werren, PhD - Professor, Biology, Univ. Rochester

 Jan 19, 2022 @ 3:30 p.m.

Marina Sharifi, MD PhD - Fellow, Medical Oncology ABIM Research Pathway, Univ. of Wisconsin

 Jan 14, 2022 @ 12:00 p.m.

Host: Wilmot Cancer Institute

Noah Salama - PhD Candidate, Advisors: Laura Calvi, M.D. and Minsoo Kim, Ph.D.

 Jan 13, 2022 @ 12:00 p.m.

Kala Hardy - PhD Candidate, Advisor: Toru Takimoto, D.V.M., Ph.D.

 Jan 06, 2022 @ 12:00 p.m.

 Medical Center | 

Alexander T. Pearson, M.D., Ph.D. - Speaker, The University of Chicago
Department of Medicine
Section of Hematology/Oncology
Knapp Center for Biomedical Discovery

 Dec 17, 2021 @ 12:00 p.m.

Host: The Wilmot Cancer Institute Seminar Series

Megan Ulbrich - PhD Candidate, Advisor: Michelle Dziejman, Ph.D.

 Dec 16, 2021 @ 12:00 p.m.

Host: Microbiology and Immunology Student Seminar

Kathy Santos, PhD; Cindy M.P. Duke, MD, PhD, FACOG - Assistant Program Manager, Protection Systems and Technologies Homeland Protection Mission Area Asymmetric Operations Sector The Johns Hopkins University Applied Physics Laboratory; Physician, Scientist, Virologist, Founder and Director of the Nevada Fertility Institute

 Dec 10, 2021 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Ruth Serra-Moreno, Ph.D.

 Dec 09, 2021 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Amelia Knudsen-Clark

Vera Gorbunova, PhD - Doris Johns Cherry Professor, Co-Director Rochester Aging Research Center

Reception to follow on the Forbes Mezzazine, 1-9580.

 Dec 06, 2021 @ 4:00 p.m.

 Medical Center | 

Shawn Murphy, PhD - Associate Professor, Dept. Obstetrics & Gynecology

 Dec 03, 2021 @ 8:30 a.m.

Catherine Pizzarello - PhD Candisate

Advisor: Kirsi Järvinen-Seppo, M.D., Ph.D.

Disturbances in the immune development during the first year of life can result in the development of atopic diseases such as asthma, eczema, and food allergy. Several environmental factors, such as exposure to farm life, have been shown to protect against the development of atopic diseases. Studies have immunophenotyped school-aged children to better understand the effects of farm life on immune system development; however few studies have immunophenotyped infants. The goal of the current study is to immunophenotype helper T (Th) cell and regulatory T (Treg) cell populations, both of which play a critical role in the development of tolerance or atopic disease, in infants from farming (low risk for allergy) or urban (high risk for allergy) lifestyle cohorts. Using the Scalable Weighted Iterative Flow-clustering Technique (SWIFT) pipeline, we have identified a novel, enriched CD25+CD127hi cluster expressing Th type 2 markers CCR4 and CRTH2 in the urban cohort at 6 and 12 months of age. This finding is consistent with the higher prevalence of allergic diseases in the urban population. Additionally at 12 months of age, farming cohort infants have increased gut homing memory Th and memory regulatory T (Treg) cell populations as well as TIGIT+ memory Tregs. Together these differences illustrate the impact of early farming lifestyle exposure on Th and Treg sub-populations in infants.

 Dec 02, 2021 @ 12:00 p.m.

 Medical Center | K307

Jayme L. Olsen - PhD Candidate

 Nov 29, 2021 @ 1:00 p.m.

 Medical Center | Class of 62' Auditorium

Host: Rochester School of Medicine and Dentistry - Genetics, Development, and Stem Cells PhD Program

Tomas Helikar, PhD - Susan J. Rosowski Associate Professor, University of Nebraska - Lincoln

Tomas Helikar, PhD - Susan J. Rosowski Associate Professor, Department of Biochemistry, University of Nebraska - Lincoln

Flyer

 Nov 29, 2021 @ 12:00 p.m.

Host: Juilee Thakar

Jacque Roberts, PhD - Professor, Professor & Interim Chair, Microbiology & Immunology

MBI 580
Seminars in Immunology
passcode: 468232

 Sep 17, 2021 @ 8:30 a.m.

Host: RIPS: Research in Progress

Minsoo Kim, PhD - Center for Vaccine Biology & Immunology

 Mar 17, 2021 @ 3:30 p.m.

Mary Caserta, MD, David Topham, PhD, Ann Falsey, MD, Nana Bennett, MD, Angela Branche, MD

 Jan 28, 2021 @ 12:00 p.m.

Patrick Reagan - Assistant Professor, Lymphoma Program at Wilmot Cancer Center

MBI 580 Research in Progress (RIPS) Seminar:

 Mar 06, 2020 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Phuong Nguyen

 Mar 05, 2020 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Cassandra Houser

 Feb 27, 2020 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Rohith Palli

 Feb 13, 2020 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Keegan Vaughn

 Feb 06, 2020 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Anuj Rattan

 Jan 30, 2020 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Jacques Robert - Professor of Microbiology & Immunology

RIPS – MBI 580 Research in Progress (RIPS) Seminar

 Jan 24, 2020 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Brad Mills

 Jan 23, 2020 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Scott Leddon

 Jan 16, 2020 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Emma Reilly

 Jan 09, 2020 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Adil Khan

 Dec 05, 2019 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Amiran Dzutsev, Ph.D. - Cancer and Inflammation Program NCI, NIH

Microbiology & Immunology Seminar Series

 Nov 25, 2019 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Felix Yarovinsky

Janelle Veazey

 Nov 21, 2019 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Rusty Elliott, PhD

RIPS – MBI 580 Research in Progress (RIPS) Seminar

 Sep 20, 2019 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

James McGuinness

Microbiology and Immunology Student Seminar MBI 501

 May 16, 2019 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Shannon Loelius

Microbiology and Immunology Student Seminar MBI 501

 May 09, 2019 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Dana Philpott, PhD - University of Toronto

MBI Seminar Series

 Apr 29, 2019 @ 12:00 p.m.

 Medical Center | Upper Auditorium (3-7619)

Host: Felix Yarovinsky

Jonathan Yewdell, MD, PhD - Laboratory of Viral Diseases, NIAID NIH

CVBI New Concepts in Immunology Seminar Series

 Apr 25, 2019 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Host: Andrea Sant

Irene Rodriguez Sanchez

Microbiology and Immunology Student Seminar MBI 501

 Apr 25, 2019 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Emily Ivey

Microbiology and Immunology Student Seminar MBI 501

 Mar 28, 2019 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Mark Niomiya

Microbiology and Immunology Student Seminar MBI 501

 Mar 28, 2019 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Andrew Martin

Microbiology and Immunology Student Seminar MBI 501

 Mar 07, 2019 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Jonathan Pinney

Microbiology and Immunology Student Seminar MBI 501

 Jan 31, 2019 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Sean Nelson

Microbiology and Immunology Student Seminar MBI 501

 Jan 17, 2019 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Deborah Fowell - University of Rochester

RIPS - Research in Progress Seminars in Immunology

 Dec 14, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Andrea Sant - University of Rochester

RIPS - Research in Progress Seminars in Immunology

 Dec 07, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Minsoo Kim - University of Rochester

RIPS - Research in Progress Seminars in Immunology

 Nov 30, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Jacques Robert

Second Friday Science Social

 Nov 09, 2018 @ 4:00 p.m.

 Medical Center | Ryan Case Method Room (1-9576)

Felix Yarovinsky - University of Rochester

RIPS - Research in Progress Seminars in Immunology

 Nov 09, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Alissa Trzeciak

Microbiology and Immunology Student Seminar MBI 501

 Nov 08, 2018 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Alessandra Araujo

Microbiology and Immunology Student Seminar MBI 501

 Oct 25, 2018 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Sergei Grivennikov, Ph.D - Fox Chase Cancer Center

Microbiology & Immunology Seminar Series

 Oct 22, 2018 @ 12:00 p.m.

 Medical Center | Upper Auditorium 3-7619

Host: Felix Yarovinsky

Daniel Barber, PhD - NIAID/DIR

New Concepts in Immunology Seminar Series

 Oct 18, 2018 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Host: Andrea Sant

Rima McLeod, MD - University of Chicago School of Medicine

MBI Seminar Series - Ritterson Lecture

 Oct 15, 2018 @ 12:00 p.m.

 Medical Center | Upper Auditorium 3-7619

Host: Felix Yarovinsky

Manuela Raffatellu, MD - University of California, San Diego

New Concepts in Immunology Seminar Series

 Sep 27, 2018 @ 4:00 p.m.

 Kornberg Medical Research Building | 3-9624

Host: Felix Yarovinsky

David Topham, PhD - Center for Vaccine Biology & Immunology

RIPS - Research in Progress Seminars in Immunology

 May 11, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Paige Lawrence - Environmental Medicine

RIPS - Research in Progress Seminars in Immunology

 May 04, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Deb Fowell, PhD - Center for Vaccine Biology & Immunology

Lung Biology Research Seminar Series

 May 01, 2018 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Michael O'Reilly

Jessica Shand - Pediatrics/Microbiology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Apr 27, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Jennifer Nayak - Pediatrics/Microbiology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Apr 20, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Jacob Finkelstein, Luis Martinez-Sobrido, Steven Gill, & Sally Quataert

Lung Biology Research Seminar Series

 Apr 17, 2018 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Michael O'Reilly

Terry Wright - Pediatrics/Microbiology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Apr 13, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Felix Yarovinsky - Center for Vaccine Biology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Mar 23, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

James Kobie - Medicine M&D-Infect Disease Unit

RIPS - Research in Progress Seminars in Immunology

 Mar 16, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Steve Gill - Microbiology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Mar 02, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Jacques Robert - Microbiology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Feb 16, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Michael "Rusty" Elliott - Center for Vaccine Biology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Feb 02, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

Yoshi Hayashi - Microbiology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Jan 26, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624

John Frelinger - Microbiology & Immunology

RIPS - Research in Progress Seminars in Immunology

 Jan 12, 2018 @ 8:30 a.m.

 Kornberg Medical Research Building | 3-9624