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NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY Antiretroviral drug therapy (ART) is the gold standard for HIV therapy for suppressing HIV infection. However, these small molecule drugs cannot eliminate the viral reservoir and thus, ART is a life-long therapy. Broadly neutralizing antibodies (bNAbs) could supplement ART and be used to reduce the viral reservoir through their Fc effector functions. While passive infusion of multiple active bNAbs can suppress viremia after ART is lifted, this strategy still requires the need for multiple infusions to maintain therapeutic concentrations of the bNAbs. We have been using adeno-associated virus (AAV) vectors to deliver HIV bNAbs, SIV bNAbs, and antibody-like inhibitors. AAV vectors provide means for long-term expression of bNAbs at concentrations capable of maintaining viral suppression via a one-time intramuscular administration. One issue that has been plaguing the field, especially in nonhuman primate models, is the development of host anti-drug antibodies and immune responses against the expressed bNAbs. We have recently demonstrated that targeting the immune checkpoint pathway is a promising target to limit the host immune response after vector administration. This work has resulted in consistent expression of two HIV bNAbs in rhesus macaques at concentrations thought to be in therapeutic range to suppress an HIV or SIV infection. Additionally, our work in developing eCD4-Ig, an antibody-like HIV entry inhibitor, has produced promising prophylaxis results in rhesus macaques against SHIV and SIV challenges. Because eCD4-Ig neutralizes all HIV-1, HIV-2, and SIV isolates and no escape mutations have been identified to date, it is a powerful inhibitor to combine with bNAbs for HIV and SIV therapy. Unlike ART, both antibodies and eCD4-Ig can kill infected cells, thus, providing a promising strategy to reduce and eliminate the viral reservoir. Therefore, we hypothesize combining AAV-delivered eCD4-Ig with antibodies would generate a unique viral reservoir upon suppression in the absence of ART, both characteristically and quantitatively. In Aim 1, we will optimize our AAV delivery strategy for multiple SIV antibodies and eCD4-Ig. In Aim 2, we will characterize and quantify the viral reservoir upon suppression when mediated by SIV bNAbs and eCD4-Ig compared to ART. In Aim 3, we will determine whether AAV-delivered SIV bNAbs and eCD4-Ig can increase the rate of viral reservoir decay compared to ART. These results would provide a foundation for AAV-delivered inhibitors as an alternative to ART and move the field closer to realizing an HIV cure.

NIMH - National Institute of Mental Health

HIV persists in central nervous system (CNS) reservoirs despite effective combination antiretroviral therapy (ART), contributing to chronic neuroinflammation and neuropathogenesis. While macrophages and microglia are known cellular reservoirs in the CNS, recent evidence suggests that infiltrating T cells also play a critical role in sustaining viral persistence. Limited access to human CNS tissues hampers our understanding of contributions of the CNS T cell reservoir in HIV neuropathogenesis. To closely examine the effects of HIV infection in the CNS, we will leverage a unique barcoded HIV system in a novel humanized mouse model to study CNS-resident viral reservoirs. Our preliminary data demonstrate that this barcoded HIV, which allows us to track and characterize virus that is being produced from different anatomic reservoirs, establishes a robust infection in both peripheral and CNS tissues, with RNA sequencing revealing upregulated type I interferon signaling and microglial activation, indicating HIV driven chronic neuroinflammation in vivo. Additionally, we have previously demonstrated in non-human primate (NHP) studies that HIV-specific chimeric antigen receptor (CAR) T cells that developed from gene modified hematopoietic stem/progenitor cells (HSPCs) can traffic to the CNS and reduce viral burden, indicating that there are ways to specifically deliver therapeutic antiviral T cells to the CNS. These findings highlight a need to define the mechanisms underlying T cell-mediated viral persistence in the CNS and to optimize CNS reservoir-targeted therapies. In these studies, we propose an integrated approach using barcoded HIV tracking, spatial transcriptomics, single-cell RNA sequencing, and integration site analysis to investigate the contributions of T cell populations in HIV persistence and inflammation in the CNS. Our central hypothesis is that T cells serve as key latent reservoirs in the CNS, promoting chronic immune activation, and that HSPC-derived CAR T cell therapy can effectively target and reduce these reservoirs. To test this hypothesis, we will: 1) Assess T cell reservoirs in the CNS during acute and chronic phase of HIV infection in humanized mice infected with barcoded HIV. 2) Investigate the contributions of T cell populations on CNS inflammation and neuropathogenesis during HIV infection. 3) Evaluate the antigen-specific T cell responses and therapeutic effects of CAR T cells on viral reservoir clearance and neuropathogenesis in the CNS. This study will provide critical insights into the role and consequences of T cell-mediated HIV persistence in the CNS and assess CAR T cells as a novel strategy for reservoir clearance and neuroinflammation reduction, advancing HIV cure strategies.

NIDA - National Institute on Drug Abuse

PROJECT SUMMARY Opioid receptors not only mediate pain relief but also act as the targets of potent exogenous opioids that are devastatingly addictive and cause overdose deaths. The principal target for both analgesia and addiction of exogenous opioids is the µ-opioid receptor (µOR). While traditionally thought to be regulated exclusively by opioids, recent work from our group has detailed an unexpected layer of complexity: endogenous neuromodulators such as endocannabinoids and oxytocin – classically associated with their own independently signaling receptors that regulate mood, pain, inflammation, and social behavior – can directly work to allosterically modulate µOR signaling. This unanticipated ligand-mediated crosstalk opens an entirely new dimension in opioid receptor pharmacology and suggests that targeting these pathways could yield novel interventions for opioid use disorder (OUD) and related conditions. The central goal of this project is to elucidate, at atomic resolution, the molecular mechanisms by which endogenous neuromodulators influence µOR structure and function. We will employ state-of-the-art cryo-electron microscopy (cryoEM) approaches to determine high- resolution structures of µOR in both its active and inactive states, bound to cannabinoids and neuropeptides like oxytocin. Critically, we will advance methodological innovations in time-resolved cryoEM to directly visualize the intermediate conformational states and the full activation/inactivation pathway of the receptor as it transitions between these endpoints. This will allow us, for the first time, to construct “molecular movies” that reveal the stepwise mechanisms by which natural modulators influence receptor activation, allostery, and signaling bias. Through these detailed structural insights, we aim to identify previously unrecognized allosteric sites and intermediate states that serve as "control points" for selective pharmacological intervention. These discoveries will inform the rational design of new therapeutic strategies that harness or mimic the brain’s own modulatory systems, offering a pathway to safer, more targeted treatments for OUD, pain, and overdose. In summary, this project will not only clarify the molecular basis of opioid receptor regulation in the brain, but will also set the stage for mechanism-driven drug discovery to address the current opioid crisis and advance our broader understanding of GPCR biology.

NCI - National Cancer Institute

PROJECT SUMMARY The Fanconi anemia (FA) pathway is involved in several key processes required to maintain genome stability. It promotes the repair of DNA lesions, such as inter-strand crosslinks (ICLs) and DNA double strand breaks. It is also involved in protecting nascent DNA from degradation and preventing the accumulation of single-strand DNA (ssDNA) gaps during DNA replication. FA pathway proteins also favor the resolution of RNA-DNA hybrids (R-loops), which form as a result of transcription. Mutations in FA pathway genes cause Fanconi anemia, a genetic disorder associated with bone marrow failure, developmental abnormalities, and an increased risk of hematological malignancies and solid tumors. Mutations in FA pathway genes also predispose to hereditary breast and ovarian cancer, and they have been observed in more than a third of somatic tumors. Current treatments for cancers with FA pathway defects often involve the use of DNA crosslinking agents or PARP inhibitors. However, these treatments can lose effectiveness over time as cancer cells develop resistance. To improve therapeutic outcomes, it is therefore critical to systematically define factors required for the survival of FA pathway-deficient cancer cells. In preliminary work, we conducted high-throughput genetic interaction studies to identify dependencies of mammalian cells deficient for FA pathway genes. This work identified synthetic lethal interactions between the FA pathway and the DNA repair genes GEN1, CIP2A and RHNO1. The main goals of this proposal are to characterize mechanistically the synthetic lethal relationships between these genes and the FA pathway and determine their relevance in cancer. In particular, we propose 1) to investigate the genetic dependency of cells deficient in the FA pathway on GEN1, CIP2A and RHNO1; 2) to define the endogenous sources of replication stress that sensitize cells deficient in the FA pathway to the loss of GEN1, CIP2A and RHNO1; 3) to explore the loss of GEN1, CIP2A or RHNO1 as a cancer vulnerability in the context of FA pathway deficiency and FA gene mutations. Our approach will utilize state-of-the-art CRISPR combinatorial knockout and base editing screens, coupled with functional characterization of genetic interactions and mutations using molecular and cell biology assays. We expect that these studies will advance our understanding of the interactions of the FA pathway with other DNA damage response pathways and identify vulnerabilities that could be exploited for the development of personalized therapies for FA pathway-deficient tumors.

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.

Department of Cultural Affairs and Special Events

TERRA FOUNDATION FOR AMERICAN ART

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.

API Food Fight Club

API Food Fight Club will partner with other community organizations to host the Chinatown-International District Block Party featuring Asian Pacific American music, arts, food, and culture. It will be held August 3, 2019 from 3 pm - 9pm at 900 S King St.

Seattle Asian American Film Festival

The Seattle Asian American Film Festival will screen free films at Hing Hay Park, 423 Maynard Avenue South on two successive Saturdays, August 18th and 25th, 2018. The films are targeted to Asian Americans in the surrounding community with the film on August 18th being screened in it's original Chinese language. The screening on August 25th will focus on the Japanese American internment during WWII. The films will be preceded by live performances and arts and crafts.

Department of Cultural Affairs and Special Events

COMMUNITY ARTS ACCESS PROGRAM - CITY MATCH

City of Newark

The City of Newark provides grants to nonprofit organizations and community groups for programs and projects that improve quality of life for Newark residents, including youth services, senior programs, arts, and neighborhood development.

Department of Public Health

This grant opportunity allows Skilled Nursing Facilities (SNFs), non-profit organizations, consumer advocacy organizations, and more to apply for funding to execute projects to improve the lives of SNF residents. Examples of projects include, but are not limited to, developing and implementing methods to increase Person-Centered Care, Infection Control Training, Arts and Engagement projects, and other topics. Examples of projects that will not be approved for CMP funding include, but are not limited to, research-only projects, projects with an indirect benefit to nursing residents, capital improvements to a facility, duplication of CMS requirements, paying for nursing home staff salaries, or high-dollar, complex technology, such as but not limited to engagement technology, telemedicine, alert systems, virtual reality, artificial intelligence, etc.  Applicants must use the template provided on the CDPH website. Projects may vary in length up to a maximum of 36 months. Award size is dependent on project request up to the allowable amount.  Keywords: Civil Money Penalty, CMP, CDPH, CMS, Skilled Nursing Facility, Reinvestment, Public Health, SNF

Department of Public Health

This grant opportunity allows Skilled Nursing Facilities (SNFs), non-profit organizations, consumer advocacy organizations, and more to apply for funding to execute projects to improve the lives of SNF residents. Examples of projects include, but are not limited to, developing and implementing methods to increase Person-Centered Care, Infection Control Training, Arts and Engagement projects, and other topics. Examples of projects that will not be approved for CMP funding include, but are not limited to, research-only projects, projects with an indirect benefit to nursing residents, capital improvements to a facility, duplication of CMS requirements, paying for nursing home staff salaries, or high-dollar, complex technology, such as but not limited to engagement technology, telemedicine, alert systems, virtual reality, artificial intelligence, etc.  Applicants must use the template provided on the CDPH website. Projects may vary in length up to a maximum of 36 months. Award size is dependent on project request up to the allowable amount.  Keywords: Civil Money Penalty, CMP, CDPH, CMS, Skilled Nursing Facility, Reinvestment, Public Health, SNF

National Endowment for the Humanities

CLASSICAL EDUCATION AND THE AMERICAN EXPERIMENT ? THE DECLARATION OF INDEPENDENCE AT 250 [IN 2025-2026, THE GREAT HEARTS INSTITUTE WILL CELEBRATE THE 250TH ANNIVERSARY OF THE DECLARATION OF INDEPENDENCE BY EXPLORING ITS ENDURING CONNECTION TO CLASSICAL EDUCATION. THE GREAT HEARTS CELEBRATE AMERICA PROJECT, "CLASSICAL EDUCATION AND THE AMERICAN EXPERIMENT: THE DECLARATION OF INDEPENDENCE AT 250, SEEKS TO DEEPEN OUR UNDERSTANDING OF THE AMERICAN MIND THROUGH A YEAR-LONG SERIES OF EVENTS, INITIATIVES, AND PUBLICATIONS. THE 250TH ANNIVERSARY OF AMERICA'S FOUNDING PRESENTS A UNIQUE AND TIMELY OPPORTUNITY TO ENGAGE THE CLASSICAL EDUCATION COMMUNITY NATIONWIDE. THROUGH A YEAR-LONG INITIATIVE, THE GREAT HEARTS INSTITUTE WILL HIGHLIGHT THE ESSENTIAL ROLE OF CIVIC LEARNING?ROOTED IN THE GREAT TEXTS AND IDEAS OF THE AMERICAN TRADITION?AS A CORNERSTONE OF CLASSICAL LIBERAL ARTS EDUCATION IN THE UNITED STATES.]

Cleveland Foundation

One of America's oldest community foundations, providing grants for arts, education, economic development, and neighborhood revitalization across Greater Cleveland.

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.

Coastal Community Foundation of South Carolina

Coastal Community Foundation of South Carolina ($300M in assets) supports nonprofits in SC through grants focused on education, environment, community development, arts. Awards range from $1,000 to $75,000.

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).

Belltown Collage Community Project

May 9th through June 7th Collage-O-Rama will be a drop-in location at Slip Gallery, 2301 1st Ave, for the public to make art and make friends, regardless of previous art experience level, with all supplies provided. The project enables free access to artists from a variety of backgrounds who are willing to share knowledge and information about resources. The approachable art form of collage allows visitors to create and display their work, even if it is their first time doing so. This project will be completd by July 31, 2025.

Colorado Creative Industries

Colorado Creative Industries provides grants to support arts and cultural programming, artist fellowships, arts education, and community-based arts projects across CO.

Colorado Creative Industries

Colorado Creative Industries supports Creative Districts — defined areas where arts and culture are developed as economic and community development tools — providing grants to certified Creative Districts across Colorado.

Colorado Creative Industries

Colorado Creative Industries provides general operating support grants to Colorado arts organizations, enabling them to deliver arts programming, build capacity, and expand access to arts and culture statewide.

Columbia Basin Trust

Columbia Basin Trust supports residents of the Columbia Basin region of BC through grants for community development, arts, environment, youth, and economic initiatives.

Peace Peloton

The Columbia City Night Market Holiday Series will bring neighbors together for two vibrant community events on November 15 and December 20, 2025. As a trusted South Seattle mainstay, the Market strengthens small businesses, prioritizes Black- and BIPOC-owned vendors, and provides a joyful, inclusive space where art, music, food, and culture thrive. With four years of proven impact, the Night Market drives critical holiday revenue for local merchants while fostering equity and belonging. The anticipated project completion date is January 31, 2026.