Grant List
Represents Grant table in the DB
GET /v1/grants?sort=-other_investigators
{ "links": { "first": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1&sort=-other_investigators", "last": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1442&sort=-other_investigators", "next": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=2&sort=-other_investigators", "prev": null }, "data": [ { "type": "Grant", "id": "16146", "attributes": { "award_id": "1I01RX005372-01A1", "title": "Enhancing Veterans' Long-COVID Care: A Cognitive-Sensorimotor Framework to Understand Gait and Balance Dysfunction", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [], "program_reference_codes": [], "program_officials": [], "start_date": "2026-01-01", "end_date": "2030-12-31", "award_amount": null, "principal_investigator": { "id": 44626, "first_name": "Keith Edward", "last_name": "Gordon", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 44627, "first_name": "Matthew J.", "last_name": "Major", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3527, "ror": "", "name": "JESSE BROWN VA MEDICAL CENTER", "address": "", "city": "", "state": "IL", "zip": "", "country": "United States", "approved": true }, "abstract": "As many as one in seven COVID-19 survivors will experience symptoms that persist more than two months after their acute illness has resolved. Growing evidence estimates that up to 30% of people who experience this chronic post-COVID disorder (aka post-acute sequelae of SARS-CoV-2 infection (PASC)) will exhibit gait and balance dysfunction. The consequences of impaired mobility are of considerable concern for the Veterans Health Administration (VHA) given that mobility is closely related to quality of life for older adults and almost half of Veterans are 65 years or older. There currently is no established VHA standard-of-care for PASC. The critical first step towards development of comprehensive clinical protocols to identify and treat PASC-related gait and balance dysfunction is understanding the contributing factors. PASC is characterized by diverse multi-organ system effects that has made it difficult to identify the causes of dysfunction. However, new data suggests frequently reported neurologic issues related to cognitive and sensorimotor impairment may be potential contributors to gait and balance dysfunction. While cognition, sensation, and muscle function can be measured in isolation, the effects of cognitive and sensory impairment on gait and balance are best detected using dual task tests (e.g., count backward by 7’s while walking) that pair cognitive and motor function or tasks performed in complex environments that limit sensory feedback and/or stress sensory-motor integration (e.g., maintaining standing balance with eyes closed). However, such assessments are not included in the current recommended PASC gait and balance screening guidelines, thereby leaving a clinical gap in knowledge when evaluating and treating Veterans and non-Veterans with PASC-related gait and balance dysfunction. Therefore, the proposed project will evaluate the effect of PASC on isolated cognitive-sensorimotor function (Aim 1), and cognitive-sensorimotor contributions to gait (Aim 2) and balance (Aim 3) dysfunction in COVID-19 survivors through an observational cross-sectional study design. Aim 1 will assess cognition, vision, proprioception, and muscle strength independent of functional task in COVID-19 survivors with and without PASC using established methods. Aim 2 will perform an instrumented assessment of gait performance of participants under a dual task scenario to stress cognition. Aim 3 will perform an instrumented assessment of postural balance under different conditions that challenge sensorimotor integration by compromising certain sensory modalities (vision, vestibular, somatosensory). A non-instrumented clinical outcome measure will also be performed as a secondary measure to evaluate a potential clinical screening tool. Based on emerging evidence, we hypothesize that COVID-19 survivors with PASC will exhibit worse cognitive-sensorimotor function, dual task gait performance, and sensory-interaction balance performance than those without PASC when accounting for age, sex, and time since acute infection. PASC-induced gait and balance dysfunction has significant clinical implications as it could compromise mobility, long-term health, and quality of life of Veterans if left unaddressed. Outcomes from this study will generate new knowledge on PASC-induced gait and balance dysfunction as related to cognitive-sensorimotor impairment, This information is critical for informing VHA PASC standard-of-cares that are currently being developed to ensure inclusion of appropriate gait and balance assessments and integrative whole-health treatments that consider the diverse mechanisms of PASC.", "keywords": [ "Accounting", "Activities of Daily Living", "Acute", "Address", "Affect", "Age", "Assessment tool", "Body System", "COVID-19 survivors", "Caring", "Chronic", "Chronic Disease", "Clinical", "Clinical Protocols", "Clinical Treatment", "Cognition", "Cognitive", "Complex", "Cost Analysis", "Cross-Sectional Studies", "Data", "Development", "Diagnostic", "Disease", "Ensure", "Environment", "Equilibrium", "Esthesia", "Evaluation", "Exhibits", "Eye", "Fatigue", "Functional disorder", "Functional impairment", "Gait", "Gait speed", "Health", "Impaired cognition", "Impairment", "Infection", "Knowledge", "Left", "Long COVID", "Measures", "Methods", "Mobility decline", "Modality", "Motor", "Movement", "Muscle", "Muscle Weakness", "Muscle function", "Musculoskeletal", "Musculoskeletal Equilibrium", "Nervous System Disorder", "Neurologic", "Outcome", "Outcome Measure", "Outcome Study", "Participant", "Pathway interactions", "Performance", "Persons", "Physical activity", "Post-Acute Sequelae of SARS-CoV-2 Infection", "Post-Concussion Syndrome", "Proprioception", "Protocols documentation", "Quality of life", "Recommendation", "Reporting", "Research", "Research Design", "Risk", "Role", "Screening procedure", "Sensorimotor functions", "Sensory", "Sensory impairment", "Short-Term Memory", "Stress", "Surface", "Symptoms", "Testing", "Time", "Treatment Protocols", "Veterans", "Veterans Health Administration", "Vision", "Walking", "acute COVID-19", "acute infection", "chronic infection", "chronic inflammation", "clinical outcome measures", "cognitive load", "cognitive process", "cost", "evidence base", "experience", "gait performance", "lens", "muscle strength", "older adult", "post-COVID-19", "research clinical testing", "screening", "screening guidelines", "sensory feedback", "sensory input", "sex", "somatosensory", "standard of care", "treatment guidelines", "vestibular system", "whole health" ], "approved": true } }, { "type": "Grant", "id": "16135", "attributes": { "award_id": "1P01AI181935-01A1", "title": "Microbiology of Treatment Shortening in Tuberculosis\"", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 44618, "first_name": "JIM P", "last_name": "BOYCE", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-05-26", "end_date": "2031-04-30", "award_amount": 3589323, "principal_investigator": { "id": 24121, "first_name": "Kyu Y", "last_name": "Rhee", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 44619, "first_name": "Dirk", "last_name": "Schnappinger", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 825, "ror": "", "name": "WEILL MEDICAL COLL OF CORNELL UNIV", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true }, "abstract": "- OVERALL Efforts to establish control of the tuberculosis (TB) pandemic face historically unprecedented challenges. In the wake of COVID-19-induced disruptions in TB healthcare-related services, TB has re-emerged as the leading cause of deaths due to an infectious disease with 2 consecutive years of the first increases in TB mortality seen in over a decade. Lacking more effective and scalable transmission blocking interventions, control of the TB pandemic will continue to rest on the clinical efficacy of chemotherapy. Unfortunately, while still therapeutically effective against 95% of newly diagnosed cases, existing chemotherapies have proven functionally far less effective due to their toxicities and months-long duration. This Program Project proposes to lay a basic-science foundation for developing treatment shortening drugs and regimens. Such studies are motivated by the empirical discovery of the treatment shortening properties of rifampin and pyrazinamide, two frontline agents whose addition enabled a nearly 3-fold reduction in treatment duration, and more recent evidence implicating phenotypically drug-resistant bacterial subpopulations as a biological determinant of treatment duration. This application brings a synergistic combination of investigators and disciplines together for a collaborative attack that mobilizes new concepts, technologies and model systems to discover and test new treatment shortening targets and strategies. Project 1 focuses on mechanisms that allow these populations to persist in patients undergoing chemotherapy. Project 2 focuses on reverse translating the treatment shortening activities of rifampin and pyrazinamide into in vitro biomarkers, mechanisms and targets. Project 3 will use innovative CRISPRi-based genetic-genetic interaction mapping to identify highly efficacious Mtb drug-target combinations. Project 4 exploits genetic approaches to define the Mtb gene products whose inactivation has the greatest potential to shorten TB chemotherapy. Core A ensures the efficient flow of information and material among these projects. Core B will combine technical advances in single-cell measurement with data integration approaches to enable single cell studies of how different subpopulations respond to treatment and/or gene inactivation. Core C will provide access to a novel paucibacillary and a drug treatment mouse model of TB relapse.", "keywords": [ "Animals", "Back", "Basic Science", "Biological", "Biological Markers", "Biological Models", "Biology", "COVID-19", "CRISPR interference", "Cause of Death", "Cells", "Clinical", "Clinical Research", "Clinical Treatment", "Communicable Diseases", "Communication", "Communities", "Discipline", "Drug Targeting", "Drug Tolerance", "Drug resistance", "Drug toxicity", "Ensure", "Face", "Fatigue", "Foundations", "Gene Silencing", "Genes", "Genetic", "Goals", "Health Care", "In Vitro", "Intervention", "Knowledge", "Maps", "Measurement", "Mediating", "Methodology", "Methods", "Microbiology", "Modeling", "Mycobacterium tuberculosis", "Newly Diagnosed", "Patients", "Performance", "Pharmaceutical Preparations", "Pharmacotherapy", "Phenotype", "Population", "Predisposition", "Property", "Pyrazinamide", "Recurrent disease", "Regimen", "Relapse", "Research", "Research Design", "Research Personnel", "Resources", "Rest", "Rifampin", "Services", "Shapes", "Technology", "Testing", "Therapeutic", "Toxic effect", "Translating", "Tuberculosis", "antimicrobial", "bacterial resistance", "chemotherapy", "clinical efficacy", "data integration", "drug development", "drug relapse", "experimental study", "gene product", "genetic approach", "in vivo", "innovation", "mortality", "mouse model", "novel", "pandemic disease", "pandemic response", "pre-clinical", "premature", "programs", "technology platform", "therapeutically effective", "transmission blocking", "treatment duration", "tuberculosis chemotherapy", "tuberculosis drugs", "tuberculosis treatment" ], "approved": true } }, { "type": "Grant", "id": "16126", "attributes": { "award_id": "1R01AI199482-01", "title": "Maternal Respiratory Infection Shapes Fetal Lung Epithelial Immune Memory: Implications for Postnatal Inflammatory Lung Diseases", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 44292, "first_name": "MERCY R", "last_name": "PRABHUDAS", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-05-11", "end_date": "2031-04-30", "award_amount": 822060, "principal_investigator": { "id": 11021, "first_name": "Hongpeng", "last_name": "Jia", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 344, "ror": "https://ror.org/00za53h95", "name": "Johns Hopkins University", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [ { "id": 44607, "first_name": "Xi", "last_name": "Ren", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3520, "ror": "", "name": "JOHNS HOPKINS UNIVERSITY", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true }, "abstract": "Maternal immune activation (MIA) during pregnancy, particularly from viral infections like SARS-CoV-2 (SCV2), poses significant risks to fetal development, resulting in long-term immune dysfunction in offspring. Our findings suggest that maternal SCV2 infection predisposes offspring to chronic inflammatory lung diseases, such as asthma, through the formation of prenatal lung epithelial immune memory linked to epigenetic modifications in key inflammatory genes like IL-33. This project aims to define the mechanisms by which prenatal lung epithelial immune memory is established and contributes to chronic inflammatory lung diseases. We hypothesize that maternal SCV2 infection disrupts the SDF-1/CXCR4 axis in fetal lung mesenchyme via maternal IL-6, leading to epigenetic changes in fetal epithelial cells, including increased chromatin accessibility at inflammatory genes such as IL-33. To test this, we will (1) investigate how the timing of maternal SCV2 infection impacts immune memory formation, (2) examine mesenchymal-epithelial cell interactions in immune memory formation, and (3) explore signaling pathways that mediate SDF-1/CXCR4-driven epigenetic changes. The results of this research will uncover novel mechanisms of non-immune cell immune memory and provide insights for developing preventive strategies for chronic inflammatory lung diseases in offspring exposed to maternal viral infections.", "keywords": [ "2019-nCoV", "Acute Respiratory Distress Syndrome", "Asthma", "CXCR4 Receptors", "CXCR4 gene", "Caring", "Cell Communication", "Cell Maturation", "Cells", "Characteristics", "Chromatin", "Cohort Studies", "Complex", "DNA Methylation", "Data", "Development", "Epigenetic Process", "Epithelial Cells", "Epithelium", "Exhibits", "Exposure to", "Fetal Development", "Fetal Lung", "Foundations", "Future Generations", "Genes", "Goals", "Human", "Immune System Diseases", "Immunologic Memory", "Inflammation", "Inflammatory", "Inflammatory Response", "Interleukin-6", "Link", "Lung", "Mediating", "Memory", "Mesenchymal", "Mesenchyme", "Modification", "Molecular", "Molecular Target", "Mothers", "Play", "Pregnancy", "Prevention strategy", "Preventive", "Production", "Regulation", "Research", "Respiratory Tract Infections", "Risk", "Role", "SARS-CoV-2 infection", "Shapes", "Signal Pathway", "Signal Transduction", "Stimulus", "Testing", "Therapeutic", "Virus Diseases", "chronic inflammatory lung disease", "cytokine", "epithelial stem cell", "fetal", "histone modification", "immune activation", "inflammatory lung disease", "insight", "lung development", "mouse model", "neonate", "novel", "offspring", "postnatal", "prenatal", "prevent", "public health intervention", "pulmonary", "respiratory", "response", "stem cell function", "viral transmission" ], "approved": true } }, { "type": "Grant", "id": "16107", "attributes": { "award_id": "1R21AI193250-01A1", "title": "Discovery of Cell Intrinsic Immunologic Adjuvants for Improving Self Amplifying RNA Vaccines Against Infectious Diseases", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 44528, "first_name": "AARON MICHAEL", "last_name": "JOFFE", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-06-12", "end_date": "2028-05-31", "award_amount": 251938, "principal_investigator": { "id": 44584, "first_name": "Priti", "last_name": "Kumar", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 44585, "first_name": "Oscar J", "last_name": "Murillo Gomez", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3508, "ror": "", "name": "YALE UNIVERSITY", "address": "", "city": "", "state": "CT", "zip": "", "country": "United States", "approved": true }, "abstract": "The COVID-19 pandemic demonstrated both the potential and limitations of mRNA-based vaccines. While very effective, current mRNA-LNP vaccines face challenges including significant reactogenicity, high dose requirements, and limited durability of immune responses. To address these shortcomings, many in the field are utilizing the unique ability of nucleic acid vaccines to express soluble mediators of adaptive immunity such as chemokines and cytokines as molecularly encoded adjuvants. While effective in preclinical models, cytokines as molecular therapies have struggled with notable toxicity and off target effects in human clinical trials. Here we propose an innovative solution which aims to enhance next-generation nucleic acid vaccines by investigating novel cell-intrinsic immunomodulators as molecular adjuvants. Our preliminary data supports this hypothesis, and the feasibility of this approach showing that self-amplifying RNA (saRNA) mediated co- expression of vaccine antigens with cell-intrinsic immunomodulator, from a single RNA molecule, results in enhanced neutralizing antibody potency and durability, and protection against viral challenge. We hypothesize that this will avoid the toxicities associated with molecularly encoded adjuvants such as cytokines, while improving the vaccine induced adaptive immune response at a significantly lower dose. The two specific aims of this proposal focus on assessing co-expression model antigens of SARS-CoV-2 Spike and Influenza A virus H5N1 Hemagglutinin with key molecules involved in DC licensing and trafficking (CD40, CD80, CCR7, and T- bet.), either (Aim 1) delivered as a LNP-saRNAantigen/imod on a single molecule or (Aim 2) co-formulated as LNP-(mRNAantigen+mRNAimod). Antibody potency, breadth, and durability will be assessed and will safety and reactogenicity. We believe that this proposal has the potential to revolutionize vaccinology through our innovative approach of harnessing cell intrinsic immunomodulators targeting DC function and development as molecular vaccine adjuvants. Our strategy aims to enhance vaccine performance while reducing doses and reactogenicity, potentially addressing key limitations of current mRNA vaccines. Success will lead to more effective and better-tolerated vaccines for emerging infectious diseases, and pandemic preparedness. Results will advance our understanding of molecular adjuvants and may establish a new platform for next-generation nucleic acid vaccines with broader applications in infectious disease prevention.", "keywords": [ "Address", "Adjuvant", "Alpha Virus", "Antibodies", "Antibody Response", "Antibody titer measurement", "Antibody-mediated protection", "Antigens", "Biology", "CD40 Antigens", "CD80 gene", "COVID-19 pandemic", "Cell Line", "Cell Physiology", "Cells", "Cellular biology", "Clinical", "Clinical Trials", "Communicable Diseases", "Data", "Dendritic Cells", "Dendritic cell activation", "Development", "Disease", "Dose", "Emerging Communicable Diseases", "Ensure", "Face", "Formulation", "Future", "Generations", "Genes", "Goals", "Hemagglutinin", "Human", "Immune response", "Immunity", "Immunologic Adjuvants", "Immunology", "Immunomodulators", "Influenza A Virus H5N1 Subtype", "Influenza A virus", "Japan", "Licensing", "Longevity", "Mediating", "Mediator", "Messenger RNA", "Modeling", "Molecular", "Molecular Vaccines", "Mus", "Nucleic Acid Vaccines", "Nucleic Acids", "Pathway interactions", "Performance", "Positioning Attribute", "Pre-Clinical Model", "Productivity", "RNA", "RNA amplification", "RNA vaccine", "Replicon", "Research", "SARS-CoV-2 antigen", "SARS-CoV-2 spike protein", "Safety", "Self Assessment", "Site", "T-Lymphocyte", "TNFRSF5 gene", "Technology", "Testing", "Toxic effect", "Transcript", "Vaccination", "Vaccine Adjuvant", "Vaccine Antigen", "Vaccines", "Viral", "adaptive immune response", "adaptive immunity", "cell type", "chemokine", "cytokine", "disorder prevention", "dosage", "experimental study", "flexibility", "frontier", "future pandemic", "immunogenicity", "improved", "in vivo", "innovation", "lipid nanoparticle", "mRNA lipid nano particle vaccine", "neutralizing antibody", "next generation", "novel", "novel strategies", "novel vaccines", "pandemic preparedness", "pandemic virus", "pathogen", "preclinical study", "response", "side effect", "single molecule", "success", "trafficking", "vaccine immunogenicity", "vaccine response", "vaccine safety", "vaccinology", "virology" ], "approved": true } }, { "type": "Grant", "id": "16101", "attributes": { "award_id": "1R01HL182777-01", "title": "Disordered mitochondrial proteostasis and alveolar epithelial repair in the aging lung", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Heart Lung and Blood Institute (NHLBI)" ], "program_reference_codes": [], "program_officials": [ { "id": 44231, "first_name": "INGRID CECILIA", "last_name": "ESPINOZA GRANDON", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-06-25", "end_date": "2028-05-31", "award_amount": 1589058, "principal_investigator": { "id": 27544, "first_name": "GR Scott", "last_name": "Budinger", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 31773, "first_name": "Seunghye", "last_name": "Han", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, { "id": 44579, "first_name": "NAVDEEP S", "last_name": "CHANDEL", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3504, "ror": "", "name": "NORTHWESTERN UNIVERSITY", "address": "", "city": "", "state": "IL", "zip": "", "country": "United States", "approved": true }, "abstract": "Pneumonia, the most common cause of death from an infectious disease worldwide, disproportionately affects the elderly. This disproportionate impact of pneumonia in older individuals became evident to all during the COVID-19 pandemic, which caused the death of nearly 7 million mostly elderly people worldwide. Furthermore, older pneumonia survivors are at increased risk for age-related disorders including persistent lung injury, skeletal muscle dysfunction leading to immobility, cognitive impairment, and dementia, highlighting pneumonia as a gateway for the compounding morbidity that limits healthspan at the end of life. We published a mechanistic model to explain the worsened lung injury and impaired lung recovery after viral pneumonia in old compared with young mice and humans. Respiratory viruses infect alveolar epithelial cells damaging the alveolar membrane. The loss of alveolar epithelial cells activates a process of repair, which is primarily mediated by alveolar epithelial type 2 (AT2) cells, the major progenitor cell population in the alveolus. AT2 cells proliferate and differentiate into alveolar epithelial type 1 (AT1) cells to restore the alveolar epithelium. Using single-cell RNA-sequencing, we and others identified a “transitional epithelial cell” population that accumulates during AT2 to AT1 differentiation. During postnatal development, we causally linked an increase in the NADH/NAD+ ratio resulting from dysfunction in complex I of the mitochondrial electron transport chain to pathologic activation of the integrated stress response (ISR) that led to the accumulation of transitional cells and death of the animal during alveologenesis. Our preliminary data reveal that loss of mitochondrial complex I function in AT2 cells of young adult mice leads to progressive fatal lung fibrosis. These findings support our hypothesis that age-related dysfunction in complex I of the mitochondrial electron transport chain increases NADH/NAD+ to induce pathologic activation of the ISR that acts via ATF4 and ATF5 to prevent alveolar epithelial repair after viral pneumonia. We will test this hypothesis in three interrelated Specific Aims. Aim 1: To determine whether age-related changes in mitochondrial complex I function or the mitochondrial NADH/NAD+ ratio in alveolar epithelial cells is necessary for the failure of alveolar epithelial repair after viral pneumonia. Aim 2. To determine whether activation of the ISR is necessary for alveolar epithelial repair after viral pneumonia. Aim 3: To determine whether activation of ATF4 alone or in combination with ATF5 in AT2 cells is necessary for the age-related failure of alveolar epithelial repair after viral pneumonia. Completion of these Aims will credential therapies targeting the NADH/NAD+, ISR, ATF4, and ATF5 to reduce the morbidity and mortality associated with viral pneumonia in the elderly.", "keywords": [ "2019-nCoV", "Adult", "Affect", "Aging", "Alveolar", "Alveolus", "Animals", "COVID-19 pandemic", "Caenorhabditis elegans", "Cause of Death", "Cell Aging", "Cell Differentiation process", "Cell Proliferation", "Cells", "Cellular Stress", "Cessation of life", "Communicable Diseases", "Complex", "Credentialing", "Data", "Dementia", "Development", "Drug Targeting", "EIF-2alpha", "Elderly", "Electron Transport", "Epithelial Cells", "Epithelium", "Exhibits", "Failure", "Functional disorder", "Gases", "Gene Expression", "Gene Targeting", "Genetic", "Human", "Immobilization", "Impaired cognition", "Impairment", "Inflammatory", "Influenza A virus", "Injury", "Link", "Lung", "Mammals", "Measures", "Mediating", "Membrane", "Mitochondria", "Mitochondrial Diseases", "Mitochondrial Electron Transport Complex I", "Modeling", "Morbidity", "Mus", "Mutation", "NADH", "NADH oxidase", "Nature", "Older Population", "Open Reading Frames", "Outcome", "Pathologic", "Pathway interactions", "Patients", "Persons", "Phosphorylation", "Phosphotransferases", "Physiological", "Pneumonia", "Population", "Predisposition", "Process", "Proliferating", "Protein Inhibition", "Proteins", "Publishing", "Pulmonary Fibrosis", "Recovery", "Risk", "Skeletal Muscle", "Survivors", "Testing", "Transitional Cell", "Transitional Epithelium", "Translational Repression", "Translations", "Viral Pneumonia", "Virus", "Yeasts", "Youth", "age related", "age related changes", "age-related disease", "alveolar epithelium", "biological adaptation to stress", "cell injury", "end of life", "epithelial repair", "functional decline", "healthspan", "influenza A pneumonia", "influenza infection", "inhibitor", "lung injury", "lung repair", "mRNA Translation", "mortality", "mouse model", "novel", "old mice", "pharmacologic", "postnatal", "postnatal development", "prevent", "protective pathway", "proteostasis", "recruit", "repaired", "respiratory virus", "response", "single-cell RNA sequencing", "stem cell population", "targeted treatment", "young adult", "young population" ], "approved": true } }, { "type": "Grant", "id": "16099", "attributes": { "award_id": "1R01HL184418-01", "title": "The role of tPA in reducing Lp(a) assembly", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Heart Lung and Blood Institute (NHLBI)" ], "program_reference_codes": [], "program_officials": [ { "id": 44576, "first_name": "LIJUAN", "last_name": "LIU", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-07-01", "end_date": "2030-03-31", "award_amount": 812747, "principal_investigator": { "id": 44577, "first_name": "Gissette", "last_name": "Reyes-Soffer", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 44578, "first_name": "Ze", "last_name": "Zheng", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3503, "ror": "", "name": "MEDICAL COLLEGE OF WISCONSIN", "address": "", "city": "", "state": "WI", "zip": "", "country": "United States", "approved": true }, "abstract": "Epidemiological, genome-wide association, and mendelian randomization studies have demonstrated that lipoprotein (a) is an independent causal risk factor for cardiovascular disease. High Lp(a) levels are associated with up to 8 times higher risk of myocardial infarction and ischemic stroke, which are thrombotic events that can occur in atherosclerotic vessels. Lp(a) consists of two main protein components that may both contribute to atherosclerosis and thrombosis: a full-length apolipoprotein B100 (apoB) moiety and an apolipoprotein (a) [apo(a)] moiety. The apoB moiety is pro-atherogenic because it is a low-density lipoprotein (LDL)-like particle with a scaffolding protein apoB. The apo(a) moiety is pro-thrombotic because it is a structural homolog to plasminogen and inhibits plasminogen activation which is the primary mechanism breaking down blood clots, a process called fibrinolysis. The plasma level of Lp(a) was thought to be mostly determined by the genetic variants of LPA gene, and therefore, its level theoretically should be stable, leading to the numerous clinical recommendations for measuring Lp(a) once in lifetime. However, recent evidence shows changes in Lp(a) levels in the same individual. These changes highlight the presence of regulatory mechanisms, beyond genetics, that regulate plasma Lp(a) levels. Fibrinolysis is initiated by a serine protease tissue-type plasminogen activator (tPA) by converting plasminogen to its active form, plasmin, which cleaves cross-linked fibrin clots. Recently we have made several observations that suggest a potential role of tPA in lowering Lp(a) levels. We have shown that: 1) hepatocytes synthesize tPA and hepatocyte-derived tPA contributes to circulating tPA concentration and fibrinolysis. 2) In patients with severe COVID-19, tPA activity decreases while Lp(a) increasing during hospitalization. Among those who survived, Lp(a) decreased and tPA enzymatic activity increased after recovering from COVID-19 symptoms. 3) The Kringle 2 domain of tPA directly binds apoB’s the N-terminus, where the Kringle IV types 5-8 domains of apo(a) also interacts with, suggesting a potential role of tPA in competing with apo(a) for its interaction with apoB. Our new preliminary data showed that 1) tPA forms complexes with apoB’s N-terminal fragments apoB9, apoB15, or apoB18 where apo(a) interacts with apoB through lysine-mediated mechanisms. 2) A lysine analog, tranexamic acid, partially blocks the interaction between tPA and apoB. 3) Silencing tPA in human primary hepatocytes increased Lp(a) in serum-free culture medium. 4) Silencing PAI1 in human primary hepatocytes increases Lp(a) levels. Based on these compelling data, in this proposal, we will test the central hypothesis that tPA inhibits Lp(a) assembly by blocking apoB binding to apo(a) using Lp(a) transgenic mice, human primary hepatocytes and human plasma samples in the following specific aims: Aim 1. To test the hypothesis that tPA blocks apoB-apo(a) interaction. Aim 2. To test the hypothesis that tPA reduces the available apoB and apo(a). Aim 3. To test the hypothesis that reducing Lp(a) by increasing hepatocyte tPA lowers atherosclerosis and improves fibrinolysis.", "keywords": [ "Affect", "Age", "Alteplase", "Antisense Oligonucleotides", "Apolipoproteins", "Aspartic Acid", "Atherogenicity", "Atherosclerosis", "Automobile Driving", "Autophagocytosis", "Autophagosome", "Binding", "Binding Sites", "Blood coagulation", "Body mass index", "COVID-19", "Cardiovascular Diseases", "Charge", "Circulation", "Clinical", "Coagulation Process", "Communities", "Complex", "Culture Media", "Cytolysis", "Data", "Endoplasmic Reticulum", "Epidemiology", "Event", "Fibrin", "Fibrinolysis", "Genes", "Genetic", "Golgi Apparatus", "Hepatocyte", "Homologous Gene", "Hospitalization", "Human", "In Vitro", "Individual", "Ischemic Stroke", "Kringles", "Length", "Lipoprotein (a)", "Low-Density Lipoproteins", "Lysine", "Lysosomes", "Measures", "Mediating", "Mendelian randomization", "Messenger RNA", "Myocardial Infarction", "Myocardial Ischemia", "N-terminal", "Patients", "Plasma", "Plasmin", "Plasminogen", "Plasminogen Activator", "Plasminogen Activator Inhibitor 1", "Process", "Proteins", "Reagent", "Recommendation", "Role", "Sampling", "Scaffolding Protein", "Serine Protease", "Serum", "Sorting", "Symptoms", "Testing", "Thrombosis", "Tranexamic Acid", "Transgenic Mice", "apolipoprotein Lp(a+)", "cardiovascular risk factor", "crosslink", "genetic variant", "genome wide association study", "high risk", "improved", "in vivo Model", "inhibitor", "lysine analog", "multicatalytic endopeptidase complex", "particle", "receptor", "severe COVID-19", "sortilin", "thrombotic" ], "approved": true } }, { "type": "Grant", "id": "16082", "attributes": { "award_id": "1P01AI198498-01", "title": "Exploiting virus and host diversity to define mechanisms of cross-species infections", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 44537, "first_name": "YAN", "last_name": "WANG", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-07-01", "end_date": "2031-05-31", "award_amount": 2000000, "principal_investigator": { "id": 8995, "first_name": "Sara", "last_name": "Cherry", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 232, "ror": "https://ror.org/00b30xv10", "name": "University of Pennsylvania", "address": "", "city": "", "state": "PA", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [ { "id": 5088, "first_name": "Ryan", "last_name": "Langlois", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, { "id": 44560, "first_name": "Michael", "last_name": "Gale", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3367, "ror": "", "name": "UNIVERSITY OF MINNESOTA", "address": "", "city": "", "state": "MN", "zip": "", "country": "United States", "approved": true }, "abstract": "Emerging viruses represent a major public health threat. This is evidenced by several zoonotic events over the last ~100 years including 1918 influenza, human immunodeficiency virus, Ebola, Zika, SARS-CoV-2, SARS- CoV-2, among others. Reemerging viruses like Dengue, West Nile, and Chikungunya also pose significant risks and the geographical range of these viruses are continuing to expand. This results in new regions becoming endemic exposing new species. The rate of virus emergence and reemergence is on the rise due to the expanding human population, land use change, and movement of animals into new habitats. Currently, we cannot predict which species are permissive and may become reservoirs in new geographical environments. Increased geographical and host range of viruses increases the odds of spillover into humans. Virus are obligate intracellular parasites that require use of host factors to complete their lifecycle. Viruses also must evade the potent antiviral immune responses which have evolved to sense and protect against virus infections. Both pro- and anti-viral host factors are under heavy selection from viruses, and their genetic sequences can vary significantly across hosts. Understanding species-specific susceptibility is essential for predicting spillover events, identifying new reservoirs, and guiding public health interventions. Furthermore, a better understanding of virus-host interactions that impact replication may also lead to new antiviral treatments. The goal of this P01 Program Project is to determine the host factors that control infection of alphaviruses and flaviviruses across mammals. We will leverage a novel resource called the “Fibroblast Zoo” which is comprised of primary dermal fibroblasts which currently contains 89 mammalian species. Fibroblasts are a relevant cell type because they are an early target of virus infection after transmission by a vector during a bloodmeal and play critical roles in sensing infection and spreading virus. While they are not an intact animal, we suggest that fibroblasts can be used as a powerful screening tool to evaluate genetic landscape of virus host interactions across diverse species. We will evaluate both pro- and anti-viral factors that govern host range across two research projects. Project 1 will reveal conserved and divergent host factors that promote infection of alphavirus and flaviviruses across species. Project 2 studies will reveal conserved and divergent mechanisms of 1) innate immune and IFN effectors, 2) alphavirus and flavivirus control, and 3) viral evasion across species. These projects will be supported by three cores, the Administrative Core (Core A) will oversee the P01 Program, Core B will distribute fibroblasts from diverse species and viruses, and generate infectivity data, and Core C will perform transcriptome and genome sequencing as well as sophisticated computational analyses. Together the linked results from the projects and cores will define mechanisms that drive cellular susceptibility to virus infections across diverse species and will inform consideration of spillover potential, and strategies for mitigating infection and disrupting zoonotic virus transmission.", "keywords": [ "2019-nCoV", "Affect", "Alpha Virus", "Alphavirus Infections", "Animals", "Area", "Biodiversity", "Cells", "Cessation of life", "Chikungunya virus", "Computer Analysis", "Data", "Dengue", "Dengue Fever", "Dermal", "Ebola", "Ebola virus", "Environment", "Epidemic", "Event", "Failure", "Fibroblasts", "Flavivirus", "Genetic", "Geography", "Goals", "HIV", "Habitats", "Human", "Immune", "Immune response", "Infection", "Infection Control", "Influenza", "Integration Host Factors", "Interferons", "Life Cycle Stages", "Link", "Mammals", "Molecular", "Movement", "Natural Immunity", "Play", "Population", "Predisposition", "Program Research Project Grants", "Public Health", "RNA Virus Infections", "Research", "Research Project Grants", "Resources", "Risk", "Role", "Screening procedure", "Spanish flu", "Structure", "Viral", "Virus", "Virus Diseases", "Virus Replication", "West Nile", "ZIKA", "Zika Virus", "Zoonoses", "arthropod-borne", "blood meal", "cell type", "chikungunya", "climate change", "design", "emerging virus", "genome sequencing", "global health", "human pathogen", "land use", "novel", "obligate intracellular parasite", "pandemic disease", "permissiveness", "predictive modeling", "programs", "public health intervention", "spillover event", "success", "synergism", "transcriptome sequencing", "transmission process", "vector", "viral transmission", "virus host interaction" ], "approved": true } }, { "type": "Grant", "id": "16081", "attributes": { "award_id": "1R43AI197624-01", "title": "Next generation multi-antigen Staphylococcus aureus vaccine enabled by proprietary mutant bacteriophage Qbeta", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 32841, "first_name": "JANE M", "last_name": "KNISELY", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-07-01", "end_date": "2028-06-30", "award_amount": 299999, "principal_investigator": { "id": 24244, "first_name": "Herbert Wanjala", "last_name": "Kavunja", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 1715, "ror": "", "name": "IASO THERAPEUTICS, INC.", "address": "", "city": "", "state": "MI", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [ { "id": 44559, "first_name": "Rachel Leigh", "last_name": "Moszyk", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3493, "ror": "", "name": "IASO THERAPEUTICS, INC.", "address": "", "city": "", "state": "MI", "zip": "", "country": "United States", "approved": true }, "abstract": "Vaccines have saved millions of lives. However, there are many diseases against which vaccines are not yet available, with the COVID-19 pandemic in the world serving as a painful reminder of the need for vaccines against emerging diseases. With the growing emphasis on vaccine safety, next-generation vaccine designs have been increasingly focusing on subunit antigens. Because subunit epitopes tend to have lower immunogenicity, immunogenic carriers are critical to deliver the desired antigen to the immune system and to enhance the immune responses. However, there are very few carriers available that have been validated in clinical studies. In this SBIR Phase I project, Iaso Therapeutics, Inc. will focus on the development of a proprietary bacteriophage mutant Qβ (mQβ) virus like particle as a platform technology for conjugate vaccine against Staphylococcus aureus (S. aureus). Currently, there are no approved vaccines against S. aureus; hence, the availability of an effective vaccine will fill this critical and urgent medical need. In Aim 1, we will evaluate the protective efficacy of our lead mQβ-PNAG26 conjugate in S. aureus pre-exposed mouse model to better mimic human clinical settings. In Aim 2, we will establish a multi-component vaccine blend that will combine mQβ-PNAG26 and mQβ- α-hemolysin and test its efficacy in mice pre-exposed with S. aureus bacteria. When successfully developed, the vaccine will have the ability to alleviate the immunopathology of S. aureus caused by the secreted α-hemolysin toxin, as well as induce opsonophagocytic clearance of the bacteria by targeting cell-wall associated PNAG antigen.", "keywords": [ "Acetylation", "Address", "Antibiotic Therapy", "Antibodies", "Antigens", "Antimicrobial Resistance", "Avidity", "Bacteria", "Bacterial Infections", "Bacteriophages", "Binding", "COVID-19 pandemic", "Capsid Proteins", "Cell Wall", "Cells", "Cessation of life", "Clinical", "Clinical Research", "Combined Vaccines", "Complement", "Conjugate Vaccines", "Control Groups", "Death Rate", "Development", "Disease", "Dose", "Epitopes", "Evaluation", "Exposure to", "Future", "Genetic Engineering", "Glucosamine", "Health Care Systems", "Hemolysin", "Hospitalization", "Hospitals", "Human", "Immune", "Immune Sera", "Immune response", "Immune system", "Immunize", "Immunoglobulin G", "Immunologics", "Infection", "Lead", "Managed Care", "Medical", "Mus", "Nature", "Pain", "Pathogenesis", "Patient-Focused Outcomes", "Patients", "Phase", "Play", "Polysaccharides", "Population", "Prevalence", "Proteins", "Public Health", "Role", "Small Business Innovation Research Grant", "Staphylococcal Vaccines", "Staphylococcus aureus", "Staphylococcus aureus infection", "Surface", "Survival Rate", "Testing", "Therapeutic", "Toxicology", "Toxin", "Treatment Cost", "United States", "Vaccination", "Vaccine Design", "Vaccines", "Virulent", "Virus-like particle", "Work", "animal safety", "clinical translation", "comparison control", "hospitalization rates", "immunogenic", "immunogenicity", "immunopathology", "infection rate", "manufacture", "methicillin resistant Staphylococcus aureus", "mouse model", "mutant", "next generation", "novel strategies", "novel vaccines", "pathogen", "phase 1 study", "poly-N-acetyl glucosamine", "protective efficacy", "secondary infection", "standard of care", "technology platform", "vaccine access", "vaccine candidate", "vaccine development", "vaccine safety" ], "approved": true } }, { "type": "Grant", "id": "16073", "attributes": { "award_id": "1R13AI200365-01", "title": "FASEB Virus Structure and Assembly Conference", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 44546, "first_name": "BARBARA L", "last_name": "MULACH", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-07-16", "end_date": "2027-06-30", "award_amount": 23500, "principal_investigator": { "id": 44547, "first_name": "Kyung H", "last_name": "Choi", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 44548, "first_name": "Sarah M", "last_name": "Doore", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, { "id": 44549, "first_name": "Joseph Che-Yen", "last_name": "Wang", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3487, "ror": "", "name": "TRUSTEES OF INDIANA UNIVERSITY", "address": "", "city": "", "state": "IN", "zip": "", "country": "United States", "approved": true }, "abstract": "Support is requested for partial funding of the 2026 FASEB Science Research Conference on Virus Structure and Assembly, to be held July 20 - 23, 2026, in Niagara Falls, New York. This biennial conference serves as the premier international forum for scientists investigating the molecular architecture, assembly, and dynamic behavior of viruses infecting hosts across all domains of life. As global viral threats continue to emerge, the ability to understand virus biology at the structural and mechanistic levels is essential for the development of vaccines, antiviral therapeutics, and surveillance tools to combat infectious diseases. The 2026 program will highlight three timely and scientifically impactful themes: (1) pandemic-causing viruses such as HIV-1, SARS-CoV-2, and Influenza, with a focus on viral entry, immune evasion, and intracellular trafficking; (2) emerging antiviral strategies, including vaccine design, small-molecule inhibitors, and bacteriophage therapy as an approach to address antimicrobial resistance; and (3) transformational technologies that are revolutionizing virus research, including cryo-electron tomography (cryo-ET), native mass spectrometry, and integrative structural biology methods capable of resolving virus-host interactions in situ. Together, these topics will shed light on the fundamental principles of virus biology while advancing translational efforts. The four- day scientific program will include ten thematic sessions, three keynote lectures, short talks selected from abstracts, two poster sessions, and structured activities designed to promote mentoring and collaboration. Approximately 150 participants are expected, representing a wide spectrum of career stages, institutions, and geographic regions. More than 30% of attendees are anticipated to be graduate students and postdoctoral researchers, who will be supported through travel scholarships and featured in short talks and flash presentations. Several professional development opportunities, such as “Career Development and Enhancement,” “Meet the Experts,” and “Meet the Sponsors” sessions, will facilitate interactions among early-career scientists, established investigators, technology developers, and industrial partners. The conference fosters a collaborative and intellectually vibrant environment that advances structural virology and supports the scientific workforce needed to address current and future infectious disease threats.", "keywords": [ "2019-nCoV", "Academia", "Acceleration", "Address", "Anti-viral Agents", "Antimicrobial Resistance", "Architecture", "Bacteriophages", "Behavior", "Biology", "Biophysics", "Biotechnology", "Collaborations", "Communicable Diseases", "Complex", "Computer Models", "Country", "Cryo-electron tomography", "Cryoelectron Microscopy", "Development", "Discipline", "Environment", "Fostering", "Foundations", "Funding", "Future", "Geographic Locations", "Goals", "Government", "HIV-1", "Immune Evasion", "In Situ", "Industrialization", "Industry", "Infectious Diseases Research", "Infectious disease threat", "Influenza", "Institution", "International", "Knowledge", "Life", "Mass Spectrum Analysis", "Mentors", "Methodology", "Methods", "Mission", "Molecular", "Molecular Virology", "National Institute of Allergy and Infectious Disease", "New York", "Oral", "Outcome", "Participant", "Postdoctoral Fellow", "Problem Solving", "Public Health", "Readiness", "Research", "Research Personnel", "Scholarship", "Science", "Scientist", "Structure", "Technology", "Therapeutic", "Training", "Training Support", "Translational Research", "Travel", "Vaccine Design", "Vaccines", "Viral", "Virus", "Virus Diseases", "antimicrobial", "antiviral drug development", "career", "career development", "career networking", "combat", "design", "falls", "graduate student", "high-resolution", "innovation", "lectures", "meetings", "novel", "novel strategies", "pandemic disease", "pathogen", "posters", "prevent", "programs", "response", "skills", "small molecule inhibitor", "structural biology", "symposium", "therapeutic target", "tool", "trafficking", "transforming virus", "translational applications", "unpublished works", "vaccine development", "vaccine strategy", "virology", "virus host interaction", "workforce needs" ], "approved": true } }, { "type": "Grant", "id": "16073", "attributes": { "award_id": "1R13AI200365-01", "title": "FASEB Virus Structure and Assembly Conference", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 44546, "first_name": "BARBARA L", "last_name": "MULACH", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2026-07-16", "end_date": "2027-06-30", "award_amount": 23500, "principal_investigator": { "id": 44547, "first_name": "Kyung H", "last_name": "Choi", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 44548, "first_name": "Sarah M", "last_name": "Doore", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, { "id": 44549, "first_name": "Joseph Che-Yen", "last_name": "Wang", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3487, "ror": "", "name": "TRUSTEES OF INDIANA UNIVERSITY", "address": "", "city": "", "state": "IN", "zip": "", "country": "United States", "approved": true }, "abstract": "Support is requested for partial funding of the 2026 FASEB Science Research Conference on Virus Structure and Assembly, to be held July 20 - 23, 2026, in Niagara Falls, New York. This biennial conference serves as the premier international forum for scientists investigating the molecular architecture, assembly, and dynamic behavior of viruses infecting hosts across all domains of life. As global viral threats continue to emerge, the ability to understand virus biology at the structural and mechanistic levels is essential for the development of vaccines, antiviral therapeutics, and surveillance tools to combat infectious diseases. The 2026 program will highlight three timely and scientifically impactful themes: (1) pandemic-causing viruses such as HIV-1, SARS-CoV-2, and Influenza, with a focus on viral entry, immune evasion, and intracellular trafficking; (2) emerging antiviral strategies, including vaccine design, small-molecule inhibitors, and bacteriophage therapy as an approach to address antimicrobial resistance; and (3) transformational technologies that are revolutionizing virus research, including cryo-electron tomography (cryo-ET), native mass spectrometry, and integrative structural biology methods capable of resolving virus-host interactions in situ. Together, these topics will shed light on the fundamental principles of virus biology while advancing translational efforts. The four- day scientific program will include ten thematic sessions, three keynote lectures, short talks selected from abstracts, two poster sessions, and structured activities designed to promote mentoring and collaboration. Approximately 150 participants are expected, representing a wide spectrum of career stages, institutions, and geographic regions. More than 30% of attendees are anticipated to be graduate students and postdoctoral researchers, who will be supported through travel scholarships and featured in short talks and flash presentations. Several professional development opportunities, such as “Career Development and Enhancement,” “Meet the Experts,” and “Meet the Sponsors” sessions, will facilitate interactions among early-career scientists, established investigators, technology developers, and industrial partners. 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