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Characterizing genetic effects on molecular phenotypes at the single-cell resolution across brain regions in the context of substance use disorder and HIV

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NIDA - National Institute on Drug Abuse

Project Summary Millions of individuals are affected with substance use disorders (SUD), posing a significant burden on these individuals, their families, and communities. There is a substantial comorbidity between SUD and HIV infection. HIV is also a risk factor for SUD because of the increased use of opioid pain medications that may lead to opioid addiction. The Single-Cell Opioid Responses in the Context of HIV (SCORCH) consortium was formed to gain insights into cellular and molecular responses in different brain regions to SUD and HIV by collecting single-cell transcriptomic and epigenomic data in affected brain regions from hundreds of human donors, as well as from animal models. It has been observed that SUD and HIV comorbidity may exacerbate cellular dysfunction beyond the effects of each condition alone, and the data generated by the SCORCH consortium provide opportunities for a comprehensive characterization of cellular states across conditions including control, HIV, OUD, and HIV+OUD. Preliminary data show substantial heterogeneity in molecular phenotypes across samples with the same exposure, e.g., HIV and SUD. Our premise is that the identifications of genetic variants mediating the effects of exposures to HIV and SUD will offer a unique angle to understand how different cell types in different brain regions respond to the exposures, and such understanding through genetic heterogeneity among individuals can lead to novel insights and clinical applications. We will apply state-of-the-art integrative methods to investigate how genetic variants affect molecular phenotypes in different cell types across brain regions with different exposure. We will accomplish this goal through three specific aims. The first aim will analyze total read counts from a transcript/isoform or peak using Bayesian methods that explicitly model shared genetic effects to borrow information across cell types and brain regions to increase statistical power. We will perform eQTL, caQTL, and isoQTL analyses. We will also leverage the multi-omic data to infer gene regulation networks and conduct grQTL analysis. The second aim will consider allele-specific analysis to complement analyses based on total counts. We will then combine allele-specific results with total read count results. To further improve statistical power, we will integrate SCORCH data with external data sets, computationally predicted effect sizes for genetic variants, and transfer known QTLs. We will develop gene expression and chromatin accessibility imputation models to facilitate genome-wide association studies. We will work with the SCORCH team to share our results with the broader scientific community. This project will be co-led by Dr. Hongyu Zhao, Dr. Mark Gerstein, and Dr. Ke Xu, who have complementary expertise covering statistical genetics/genomics, computational biology, single-cell analysis, SUD genetics, and HIV research.

Up to $2.3M
2030-02-28
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Characterizing HIV reservoir in HIV-2, and HIV-1 and HIV-2 dual infections

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NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY The persistence of latent viral reservoirs is a major obstacle to curing HIV, as it causes viral rebound when antiretroviral therapy (ART) is interrupted. Current strategies for an HIV cure, such as "shock and kill," "block and lock," broadly neutralizing antibodies, chimeric antigen receptors, and therapeutic vaccines, focus largely on subtype B and overlook Africa, which bears the highest burden of HIV. Africa, home to two-thirds of global HIV cases, has significant genetic diversity in HIV subtypes, including HIV-1, recombinant forms, and HIV-2. HIV-2, found mainly in West Africa, constitutes 10–20% of regional HIV cases, yet little is known about its latent reservoirs, particularly in dual HIV-1/2 infections. This study aims to address this gap by investigating HIV-2 latent reservoirs and their interactions with HIV-1 in dual infections, focusing on a cohort in Ghana. A cohort of 74 virologically suppressed individuals with dual infections will be used. The team’s expertise includes developing assays to quantify viral DNA and RNA specific to HIV-2. Aim 1 focuses on quantifying reservoir sizes in CD4+ T-cell subsets (central, transitional, and effector memory) and monocytes across HIV-1, HIV-2, and dual infections. Previous studies have explored reservoirs in ART-naïve people living with HIV-2 but not in virologically suppressed or dual-infected individuals. Methods include cell-associated DNA PCR, RNA analysis, quantitative viral outgrowth assays (QVOA) and intact proviral DNA assay (IPDA). Aim 2 will create an HIV-2 latency model using cell lines like Jurkat and THP-1 and test latency-reversing agents (LRAs) on ex-vivo samples from virologically suppressed people. The team will adapt existing fluorescence-based tools for HIV-2 and measure viral reactivation using gag mRNA quantification. The outcomes will provide critical insights into the HIV-2 reservoir and its impact on HIV-1 in dual infections, laying the groundwork for cure strategies that extend to the USA and globally, as HIV-2 has been identified in other regions, including the USA, due to migration. Understanding HIV-2 reservoir dynamics and latency reactivation will inform the development of new ways to tackle HIV-1 which will benefit PWH in the USA as well. Findings from the study could advance global HIV cure research on reservoir characteristics, measurement tools, and therapeutic approaches that address different viral subtypes and dual infections. The proposal aligns with exploratory R21 mechanisms and has the potential to significantly advance HIV cure research in the USA and globally.

Up to $146K
2028-06-30
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Child Health Research Career Development Award (CHRCDA) Program at Children's National

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NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development

Abstract The Child Health Research Career Development Award (CDRCDA) Program was first established at Children’s National Hospital in 2000, and over the past 24 years, we have successfully trained 30 Scholars. The purpose of the program is to facilitate the development of successful basic, translational, and clinical research careers for junior faculty members in pediatrics across the T0-T4 spectrum. The rationale for the program is that while many opportunities exist to use molecular biology, biomedical engineering, and translational science to advance treatment of pediatric diseases, the comprehensive scientific knowledge and practical experience that are required to capitalize on these opportunities are often deficient among young pediatrician-investigators who have recently finished clinical training. The CHRCDA addresses this need by providing protected time for nascent scientists during their initial academic appointment. In our program, scholars: 1) take coursework in basic, translational, or clinical science areas relevant to their research; 2) learn state-of-the art laboratory and computational methodologies; 3) develop preliminary data under the supervision of established mentors that will lead to submission of independent NIH grant applications; and 4) learn to effectively advance accomplishments in basic, translational, and clinical research into improvements in child health. To accomplish these goals, the CHRCDA scholars spend at least 75% effort honing these skills under the mentorship of established mentors over a 3-4 year period. During this period, each of the above tasks will be addressed in a systematic fashion, including participation in a core curriculum in research methodology and biostatistics, training in responsible conduct of research, and performance of increasingly independent research under senior investigators. We fund 2-3 Scholars annually and match these scholars with senior mentors within four scientific affinity groups: neuroscience, molecular genetics, cancer and immunology, and biomedical engineering. The administrative structure includes a Principal Investigator/Program Director, a Training Director, an Executive Committee, and an external Advisory Committee. The outcomes of this program are measured by the products of the scholars’ subsequent academic careers: publications and independent external grant support. Recent innovations to our program include: expansion of funded research to include T2-T4 science with recruitment of a cadre of appropriate mentors, new pipeline programs to increase our pool of candidates including two R38 awards to fund research among pediatric residents and significant capital investments including the new Children’s National Research and Innovation campus. This administrative supplement is necessary to sustain the CDRCDA program during an unanticipated funding gap, ensuring uninterrupted support for scholars and continued program operations until a future funding opportunity is released.

Up to $297K
2027-03-31
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Cholinergic signaling for sensorimotor acquisition and implicit learning

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NIMH - National Institute of Mental Health

PROJECT SUMMARY In a dynamic environment, learning is an evolutionary advantage. When faced with a novel situation, animals that adapt their behavior appropriately may live to reproduce another day. Associative learning requires linking distinct events across time, such as a sensory event with a motor command that results in the desired outcome. How are flexible sensorimotor associations implemented in the brain? The brain regions supporting the encoding of these events are broadly distributed suggesting that learning- related plasticity would benefit from neural mechanisms that operate across multiple timescales and brain regions. Ascending neuromodulatory systems—with their broad projection architecture and multiple timescales of activity—fulfill these criteria and could serve as a potent mechanism to link the different sensory, motor and outcome components. More specifically, the cholinergic basal forebrain (CBF) is the ideal candidate to support rapid learning-related plasticity across multiple cortical regions. This builds on a robust literature showing a pleiotropic role of the CBF to establish both sensory and motor cortical plasticity. Additionally, CBF neurons respond precisely to reinforcement, movement, and sensory events. The overall hypothesis is that the CBF phasic activity serves as a ‘teaching’ signal, locally integrating distinct events, and then projecting conjoint signals (i.e., sensory-motor contingencies) to recipient regions on the timescale of contingency acquisition. The mentored phase will exploit a novel behavioral approach that isolates the timing of acquisition of novel sensorimotor contingencies combined with state-of-the-art optical and physiological tools to test this specific hypothesis. Aim 1 will determine the spatiotemporal dynamics of cholinergic signaling to the Auditory Cortex (AC) and Motor Cortex (MC) during early task acquisition. Aim 2 will identify the causal role of CBF in associative audiomotor acquisition. In the R00 phase this framework will be expanded to implicit learning, when previously acquired sensorimotor contingencies are subject to rapid changes. Aim 3 will determine the role of CBF in implicit learning of auditory regularities. Using a combination of state-of the art optical tools, cell-type specific and temporally precise optogenetics and custom computational analysis and tools, this project unveils the role of cholinergic inputs to distinct cortical targets in learning. There is growing evidence that hearing loss and dementia are tightly linked. Cholinergic circuits play a prominent role in essential cognitive functions which are impacted during cognitive decline. Interestingly, it is one of the earliest regions to exhibit neurodegeneration in Alzheimer’s disease. Understanding how cortical networks are modulated by cholinergic inputs to produce the appropriate behavior will advance our understanding of basic cognitive functions and help develop targeted approaches to fend-off cognitive decline.

Up to $117K
2028-07-31
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Clinical Assay to Accurately Profile and Monitor the HIV-1 Reservoir in Chronic-treated Individuals to Guide Treatment Decisions

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NIAID - National Institute of Allergy and Infectious Diseases

Project Summary/Abstract Public Health Problem. According to the World Health Organization (WHO), approximately 39 million people are currently living with HIV worldwide. Out of these, about 1.3 million were newly infected in 2022 alone. Moreover, around 630,000 people died from AIDS-related illnesses in the same year. Despite significant advances in therapies and accessibility to care and prevention methods HIV remains a global health challenge. The HIV epidemic has had a severe impact on vulnerable populations, exacerbating existing inequalities. Women and girls are disproportionately affected, accounting for over half of all new HIV infections globally. Despite antiretroviral (ART) initiation upon HIV diagnosis recommended by the 2019 U.S. guidelines, the current chronic-treated and untreated HIV-infected population is >375,000 people in the U.S. alone, and HIV continues to be routinely diagnosed during chronic infection. How Our Product Meets Unmet Needs. Jan Biotech has developed a nonezymatic, chemical amplification and direct detection assay for HIV RNA. The HIVLatentDetect assay provides quick, sensitive, and quantitative measurement of cell-based HIV RNAs in HIV-infected individuals who are fully suppressed under antiretroviral treatment, including for 100% of acute/early HIV-infection treated individuals, for which QVOA, qPCR, ddPCR, IPDA, and single viral copy assays show a ≥25% rate of assay failure or no detection. Jan Biotech’s HIVLD assay provided an unprecedented 0.97 (p-value≤0.0001) predictive value for time to HIV viral rebound after antiretroviral treatment interruption for the acute/early treated cohort in the AIDS Clinical Trials Group (ACTG) A5345. Jan Biotech’s assay would provide a much needed change to HIV standard of care, from viral load testing to detection of reservoir size predictive of, and prior to, plasma viral load changes. HIVLD provides a novel minimal residual disease (MRD) measurement to allow patients and clinicians to make earlier decisions for improving patient care. An MRD assay that captures the replication-competent fraction of chronic HIV reservoirs will allow safer participant involvement in clinical trials investigating new and potential cure or remission treatments. In the long term, HIV MRD testing will facilitate efforts to achieve a functional cure or fully eliminate HIV. Summary of Approach. The proposed work would allow Jan Biotech to expand the assay’s predictive value for time to HIV viral rebound after treatment interruption for the vast chronic-treated HIV-infected population, and to investigate the assay’s value for novel minimal residual disease (MRD) measurements to allow patients and clinicians to make earlier decisions for improving patient care and monitoring response of individual’s chronic HIV reservoir to potential cure treatments. Jan Biotech’s assay of all participating ACTG A5345 assays best captures the functional differences in the HIV reservoir leading to differences in viral rebound time between chronic- and acute/early-treated populations. Collaborators and Unique Resources. Jan Biotech, Inc., with expertise in molecular diagnostic development, will continue to collaborate with Dr. John W. Mellors, University of Pittsburgh School of Public Health; Dr. Michael Keefer, University of Rochester; Dr. Harris Gelbard, Director of the Center for Neurotherapeutics Discovery (CND) and Professor of Neurology, Pediatrics, Neuroscience and Microbiology & Immunology at the University of Rochester Medical Center; and the IVQAC team, led by Dr. Thomas Denny. Specific Aims Specific Aim 1 (Phase I): Develop HIVLD assay to differentiate chronic-treated HIV-1 subpopulations Specific Aim 2 (Phase II): Assay validation using ACTG clinical trial chronic-treated samples Specific Aim 3 (Phase II): Establish large scale clinical relevance for chronic HIV reservoir characterization Specific Aim 4 (Phase II): Software validation and verification for cHIVLD assay analytics Market after Completion. The goal of the proposed work is to develop this very promising technology to serve the vast chronic-HIV population by performing needed testing through HIV treatment interruption and large-scale population studies with well-characterized samples. The chronic-HIVLD assay (cHIVLD) is ideal for routine HIV testing, where it will provide minimal residual disease (MRD) measurements to allow patients and clinicians to make earlier decisions for improving patient care, and for HIV cure trial and research use to monitor the response of individuals’ chronic HIV reservoir to potential cure treatments.

Up to $300K
2027-01-31
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Clinical Translation of MR Cytometry

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NCI - National Cancer Institute

PROJECT SUMMARY This Academic-Industrial Partnership (AIP) grant aims to translate the MR cytometry imaging technique into a push-button imaging tool on clinical MRI platforms. MR cytometry imaging is an innovative, diffusion MRI based method that non-invasively measures mean cell size in vivo, thereby providing a powerful new way to characterize tissues for clinical applications. Investigators at Vanderbilt University Medical Center (Vanderbilt) and the University of Washington in Seattle (UW) will team up with Philips Healthcare (Philips), a major vendor and supplier of clinical MRI scanners, to optimize and implement innovative pulse sequences, and to integrate automated data analyses into Philips’ commercial platform that can be deployed widely to further assessments of the clinical role of MR cytometry imaging, particularly in breast cancer. The project builds on several years of previous NIH-funded research on diffusion MRI and a long-standing cooperation between Philips and Vanderbilt investigators. The proposal aims to fill the gap by bringing both the academic (Vanderbilt and UW) and industry (Philips) partners together to translate the MR cytometry imaging to state-of-the-art commercial platforms. This perfectly matches the goal of PAR-25-079 (Academic-Industrial Partnerships (AIP) to Translate and Validate In Vivo Imaging Systems) to “identify and translate a novel technological solution towards detection /diagnosis or treatment of cancers”. We hereby identify the following specific aims: Aim 1 [prototype development] The Philips team will develop a prototype of the MR cytometry imaging tool for end users on their commercial MRI platform, including both data acquisition using oscillating gradient spin echo (OGSE) sequences and automated data analyses of MR cytometry imaging on Philips’s clinical platform. Aim 2 [protocol optimization]: The Vanderbilt team will further optimize MR cytometry imaging protocols for the most commonly-used gradient performances, particularly for breast cancer imaging, and develop a quality control (QC) protocol including a novel breast tumor cell size phantom to ensure the accuracy and stability of diffusion MRI and MR cytometry imaging measurements. Vertebrate animal models will be needed to generate three types of breast tumors with distinct mean cell sizes, which will then be dissociated into fixed cells to create the cell size phantom. This approach will allow the phantom to mimic the realistic cellular composition and size distribution of breast tumors, including cancer cells, immune cells, and stromal cells, making it well suited as a QC phantom for MR cytometry in breast imaging. Aim 3 [multi-site evaluation]: The product prototype of MR cytometry imaging will be comprehensively evaluated for accuracy, intra- and inter-session repeatability in breast cancer patients at multiple sites, including Vanderbilt Institute of Imaging Science, Vanderbilt Hospital, and UW Hospital. Upon completion, a reliable, easyto-use, and fully automated product prototype of MR cytometry imaging will be developed on Philips’s state-ofthe-art clinical MRI platform for end users in clinics. This provides a basis for more widespread applications of MR cytometry imaging in future cancer clinical trials.

Up to $695K
2031-06-30
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

CMV reactivation in the vasculature of people with HIV drives T cell responses

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NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY/ABSTRACT Cardiovascular disease (CVD) is the leading cause of death in the United States and worldwide. People with HIV (PWH) with virus suppression on antiretroviral therapy (ART) have a 2-fold increased risk of developing CVD compared to people without HIV (PWoH), even when controlling for age and traditional CVD risk factors. One factor that may contribute to the increased CVD in PWH is cytomegalovirus (CMV) coinfection. Nearly all PWH and about half of all adults without HIV in the United States have CMV, which is independently linked to CVD. In preliminary spatial transcriptomic analyses of vascular tissues of PWH and PWoH, all of whom have peripheral artery disease, we find that the proportion of myeloid cells in regions of interest (ROIs) across arteries is significantly higher in tissues from PWH. CMV can reactivate from latently-infected monocytes as they differentiate into macrophages, and virological and immunological evidence suggests that PWH have more frequent CMV reactivation events than do PWoH, so the cardiopathogenic effects of CMV may be more pronounced among PWH due to the increased numbers of macrophages harboring replicating CMV. We hypothesize that CMV reactivation in infiltrating macrophages provides antigenic signals for CMV-reactive T cells in vascular tissues. We will use the following Specific Aims to test this hypothesis. Aim 1: To define the spatial context of CMV expression in vascular tissues of PWH and PWoH. In Aim 1, we will test this hypothesis by (1) defining the spatial context of CMV expression in situ in vascular tissues of PWH and PWoH with and without CVD, (2) quantifying CMV expression in macrophages in vessels from PWH and PWoH with and without CVD, and (3) confirming spatial relationships of CD4 and CD8 T cells and CMV-expressing target cells in the vasculature. Aim 2. To determine if serum-derived MDMs from PWH with CMV are more effective at activating and presenting CMV antigens to T cells than are MDMs from PWoH with CMV. In Aim 2, we will use in vitro experiments to determine if serum-derived MDMs from PWH with CMV, which preserves the influence of systemic inflammatory mediators, are more effective at activating autologous T cells than MDMs from PWoH with CMV. Then, we will determine if that activation is due to CMV antigen presentation by the serum-derived MDMs, and whether statin treatment of the MDMs, which inhibits CMV replication in vitro, directly impairs their T cell activating capacity. Our studies may define mechanisms whereby chronic viral infection drives T cell- mediated vascular pathology and may identify novel targets beyond traditional risk factors to prevent/treat CVD in PWH and PWoH. Furthermore, understanding the role of CMV in CVD, and whether its activity is susceptible to statins, will help inform the interpretation of the A5332/REPRIEVE (pitavastatin) and A5383/ELICIT (letermovir) trials in PWH.

Up to $234K
2028-01-31
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Cocaine and cannabinoids antagonize ART efficacy that promotes HIV infection and inflammatory responses at the maternal-fetal interface

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NIDA - National Institute on Drug Abuse

PROJECT SUMMARY/ABSTRACT Despite the effectiveness of antiretroviral therapies (ART) in reducing vertical transmission, maternal HIV infection and ART exposure during pregnancy is associated with immune dysregulation in mothers, along with inflammation and significant pathology in the placenta. Compounding these risks is the increasing prevalence of substance abuse among pregnant women and people living with HIV. Compared with the general population, HIV-positive women had higher use of marijuana (15% vs 7%) and cocaine/crack (17% vs 0.1%), and recent findings suggest that 6-18.3% of pregnant women report using illicit drugs throughout gestation. Despite this increase, little is known about the impact of comorbid substance use and HIV/ART on the placenta. In this study we seek to fill this critical knowledge gap by elucidating the mechanisms driving placental dysfunction in pregnant women living with HIV with comorbid substance use and examine how cocaine and/or cannabis use may exacerbate viral infectivity, inflammation, and ART efficacy at the maternal- fetal interface. We hypothesize cocaine and cannabis polysubstance use antagonize placental ART transport and metabolism through PXR signaling, which promotes HIV replication, inflammatory responses, and placental abnormalities associated with adverse maternal and fetal outcomes. We will address this by evaluating: pharmacologic mechanisms by which comorbid substance use and HIV alter ART placental efficacy (Aim 1), immunologic and virologic mechanisms underlying effects of comorbid substance use and HIV/ART on the placenta (Aim 2), and evaluate whether HIV, ART and/or comorbid substance use is associated with dysfunction and inflammation in placentae and maternal blood from HIV (+) and (-) pregnancies (Aim 3).

Up to $683K
2031-02-28
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Collaboratory of AIDS Researchers for Eradication (CARE)

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NIAID - National Institute of Allergy and Infectious Diseases

Abstract Since its inception in 2011, the Martin Delaney Collaboratory program has made important advances towards a cure for HIV. In response to the Martin Delaney Collaboratories (MDC) for HIV Cure Research RFA, we seek to continue to advance the field by discovery of successful modalities to cure HIV infection. We will expand our expertise and work toward a better understanding of persistent HIV infection, the discovery of novel approaches to disrupt latency, methods to clear the HIV reservoir, and identification of strategies to control viral rebound. By building on the significant advances that we have made to develop, implement, and execute a suite of pre-clinical experiments that represent the most advanced and novel concepts, we will continue to pursue our central unifying hypothesis that reversing HIV latency such that viral proteins are expressed, in parallel with interventions that speed the clearance of cells emerging from latent infection, will ultimately lead to eradication of persistent HIV infection. In parallel to the efforts to clear the infection, we will pursue interventions to prevent rebound of viremia after ART interruption. We will leverage a broad portfolio of tools from both academic and industry partners, and apply new discoveries, demonstrating proof-of-concept for clinical initiatives. We will engage academic scientists and clinicians, industry investigators, and the community to a) define novel targets to destabilize proviral genomes that persist despite antiretroviral therapy (ART) b) define novel approaches to block proviral establishment c) develop and deploy novel effectors to clear viral reservoirs, d) delineate effective strategies to prevent rebound viremia that might emanate from such reservoirs after ART is discontinued and e) create bridges to the community to improve the understanding of and access to HIV cure research and clinical trials. Our initial efforts will focus on biology discovery to illuminate new host targets for latency reversal, and the validation of the novel biological concept of latency prevention. Universal strategies for proviral control or clearance will be developed and tested, including those based on HLA-E targeting, eCD4, and CD4 mimetics. Our major recent advance in latency reversal via NF-kB signaling will be further developed in both non-human primate and humanize mice models, in combination with candidates to clear infected cells. We envision an iterative process with insights gained in ex vivo and pre-clinical studies, carried forward to enhance the next step in clinical development and, importantly, fed back to scientists to validate assays or hypotheses, and explore new directions. As we have done in the past, we will develop human clinical trials to address questions and test concepts developed in our work through funding mechanisms distinct from CARE. We are dedicated to working together in a nimble program, with our research direction following our discoveries. Together we will catalyze advances that will ultimately lead to the eradication of HIV infection.

Up to $5.3M
2028-06-30
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Columbia University-Weill Cornell Medicine CFAR (CU-WCM CFAR)

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NIA - National Institute on Aging

PROJECT SUMMARY: OVERALL The Columbia University (CU) – Weill Cornell Medicine (WCM) Center for AIDS Research (CFAR) is a partnership between two large New York City (NYC) academic institutions, each with an expanding investment in HIV research and connected by the NewYork-Presbyterian hospital system, which spans four NYC counties designated as priority high-burden jurisdictions by the US Ending the HIV Epidemic (EHE) initiative. The overall specific aims of the CU-WCM CFAR are to (1) catalyze innovative, interdisciplinary, inter-institutional HIV research that addresses key HIV research priorities for ending the epidemic in NYC and beyond; (2) engage and support career development of HIV researchers, including early-career investigators (ECIs) and investigators new to HIV; and (3) advance community-engaged participatory research that promotes health for all people. The CU-WCM CFAR will accomplish these goals by establishing, engaging, and working through six Cores: The Administrative Core will provide leadership and management; implement strategic planning; and stimulate communication, collaboration, and capacity building. The Developmental Core will provide grant funding awards; mentoring and career development for new investigators; and provide resources, training, and feedback for mentors to improve their skills. The Structural Immunology Core will provide state-of-the-art imaging and immunological technologies; molecular structure determination; and bioinformatics to understand antibody-virus co-evolution, and structural modeling. The Virology Core will provide specialized assays to measure virus replication, infectivity, and cell susceptibility to infection; comprehensive reservoir characterization; and training in these methodologies. The Clinical Research Core will provide consultative support across the course of a study ranging from study design and biostatistical planning to participant recruitment, and data analysis. The Behavioral, Implementation and Community Sciences Core will support investigators engaged in behavioral, implementation, health services, and community science research and catalyze bi-directional collaborations with communities. We also will establish a Scientific Working Group – Integrating Systems of Care to End the HIV Epidemic – that will bring together a group of dynamic multi-sector collaborators to develop a robust research agenda that addresses fragmentation of care for HIV, mental health, and substance use care co-morbidities. The CU-WCM CFAR will add value to our institutions’ existing strong research portfolios through scientific leadership and strategic planning that builds synergistic new collaborations, enhances community engagement on HIV research and health, and supports innovation and research productivity as well as the next generation of leading HIV researchers.

Up to $2.5M
2031-04-30
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

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