Project Grant R01AI186611
- This $564,001 project grant from the National Institutes of Health's National Institute of Allergy and Infectious Diseases will fund research on membrane-associated RING CH (MARCH) proteins and their role in restricting HIV-1 infection. MARCH proteins are a family of ubiquitin ligases that regulate membrane receptors and have been shown to restrict HIV-1 and other retroviruses by blocking viral envelope incorporation into budding virions. The research foundation for the State University of New...
- This Project Grant award from the National Science Foundation (NSF) under the Biological Sciences (CFDA 47.074) Federal Grant Program provides $987,566 to the University of California, Los Angeles (UCLA) to conduct research on viral self-assembly, from test tube to cell cytoplasm. The award period runs from December 15, 2024 to November 30, 2028. The key objectives of this project are to elucidate the differences between in vitro and in cellulo viral processes by progressively adding molecules...
- This $536,943.46 Project Grant from the National Institutes of Health National Institute of Allergy and Infectious Diseases funds research at The Scripps Research Institute-Florida on identifying host factors that regulate HIV latency and reactivation. The grant supports three aims over a six-month period: defining the roles of proteins P32, FUBP3, and PHB2 in HIV transcription and chromatin structure; investigating protein complexes associated with P32, FUBP3, and PHB2 and their interaction...
- This $125,888 Project Grant award from the National Science Foundation (NSF) Mathematical and Physical Sciences (CFDA 47.049) program supports research by Yale University to investigate how the mechanical properties of host cells impact the infection and integration of the human immunodeficiency virus (HIV). The key objectives are to: 1) examine how HIV infection affects the mechanical and morphological attributes of the host cell nucleus, and 2) determine how the mechanical environment of the...
- The National Institutes of Health's National Institute of Allergy and Infectious Diseases awarded a $2.3 million Project Grant to the University of California, Davis to fund research targeting CD4 T follicular helper cells for enhancing HIV vaccine-induced humoral immunity. The two-year award, issued on May 12, 2021 under the Allergy and Infectious Diseases Research program (CFDA 93.855), will support preclinical studies in rhesus macaques to better understand the immunological mechanisms...
- This Project Grant award, provided by the National Institute of Allergy and Infectious Diseases (NIAID) under the Allergy and Infectious Diseases Research program (CFDA 93.855), supports research to investigate the dynamics and evolution of HIV Gag and GagPol processing. The $752,745 award aims to use molecular dynamics simulations, single-molecule FRET imaging, and cryo-electron tomography to probe the structure and dynamics of Gag and GagPol that enable ordered processing by the viral...
- This Project Grant, awarded by the National Institute of Allergy and Infectious Diseases (NIAID) under the Allergy and Infectious Diseases Research program (CFDA 93.855), supports research to develop novel antiviral compounds targeting lenacapavir-resistant HIV strains. The $149,190 award to Emory University, effective December 25, 2025, through June 30, 2029, funds the characterization and optimization of three newly developed capsid effectors (CEs) that demonstrate superior efficacy against...
- The National Institutes of Health National Institute of Allergy and Infectious Diseases awarded $852,121.24 to The Scripps Research Institute-Florida under the Allergy and Infectious Diseases Research program (CFDA 93.855) for the period of July 22, 2021 through October 31, 2021. The project aims to identify host factors that regulate HIV latency and reactivation in order to develop strategies for durable HIV silencing. The grantee will define the roles of three identified host factors, P32,...
- Federal Project Grant Award Summary The National Institute of Allergy and Infectious Diseases (NIAID) awarded a $713,107 Project Grant to the Regents of the University of Minnesota on February 20, 2026, under the Allergy and Infectious Diseases Research program (CFDA 93.855). The research project, entitled "Molecular Determinants and Vulnerabilities of HIV-1 Spread by Cell-to-Cell Transmission," will be conducted at the University of Minnesota in Minneapolis through January 31, 2031....
- Grant Award Summary Emory University received a $153,560 Project Grant from the National Institute of Allergy and Infectious Diseases (NIAID) under the Allergy and Infectious Diseases Research program (CFDA 93.855), effective October 11, 2026, with completion scheduled for August 31, 2029. The research initiative focuses on assessing the impact of HIV envelope glycoform conservation across HIV clades on broadly neutralizing antibody (bNAb) recognition. This research addresses a critical gap in...
VIRAL AND CELLULAR DETERMINANTS OF HIV-1 ASSEMBLY - THE MAJOR GOAL OF THIS APPLICATION IS TO DEFINE VIRAL INTERACTIONS WITH HOST PATHWAYS THAT ARE ESSENTIAL FOR THE ASSEMBLY OF INFECTIOUS HIV-1 PARTICLES. WE PREVIOUSLY IDENTIFIED RAB11-FIP1C (FIP1C) AS A KEY ADAPTOR PROTEIN REQUIRED FOR HIV-1 ENVELOPE PROTEIN (ENV) TRAFFICKING AND PARTICLE INCORPORATION, A FINDING THAT ESTABLISHED THE MODEL STATING THAT HOST RECYCLING PATHWAYS ARE REQUIRED FOR PARTICLE INCORPORATION. RECENT WORK FROM OUR LABORATORY HAS EXTENDED THIS MODEL, DEFINING THE ROLE OF KIF16B IN ENV TRAFFICKING AND IDENTIFYING DISCRETE MOTIFS WITHIN THE ENV CYTOPLASMIC TAIL THAT ARE ESSENTIAL FOR RECYCLING AND PARTICLE INCORPORATION. PRELIMINARY DATA PRESENTED HERE NOW IDENTIFIES THE TUBULAR RECYCLING ENDOSOME (TRE) AS A MAJOR NEW COMPONENT OF THE RECYCLING MACHINERY INVOLVED IN PARTICLE INCORPORATION OF ENV. TRE COMPONENTS INCLUDING MICAL-L1 AND EHD1 WERE SHOWN TO BE ESSENTIAL FOR ENV TRAFFICKING AND INCORPORATION INTO PARTICLES. REMARKABLY, DISRUPTION OF TRE TRAFFICKING SEVERELY DEPLETED ENV FROM PARTICLES, BUT ONLY IN THOSE CELLS THAT HAVE BEEN SHOWN TO BE NONPERMISSIVE FOR INCORPORATION OF CYTOPLASMIC TAIL (CT)-DEPLETED ENV. THUS, THIS PATHWAY HOLDS THE KEY TO UNDERSTANDING THE CONTRIBUTION OF THE ENV CT TO THE RECYCLING AND PARTICLE INCORPORATION OF ENV. EXPERIMENTS IN AIM 1 WILL DEFINE ESSENTIAL COMPONENTS OF THE TRE THAT CONTRIBUTE TO ENV TRAFFICKING, EXAMINING EHBP1, RAB10, SYNDAPIN2, AND MICAL-L1. IN AIM 2, THE CRITICAL ROLE OF EHD1-MEDIATED SCISSION FROM THE TRE IN ENV TRAFFICKING TO THE PM SITE OF ASSEMBLY WILL BE DEFINED USING CELLULAR/BIOCHEMICAL AND IMAGING APPROACHES. A UNIQUE FAP-TAGGED ENV CONSTRUCT WILL BE EMPLOYED TO VISUALIZE AND QUANTIFY ENV TRAFFICKING FROM THE TRE TO THE PM IN LIVE CELLS. AIM 3 WILL DETERMINE THE MECHANISMS RESPONSIBLE FOR CELL TYPE- DEPENDENCE OF INCORPORATION OF ENV, USING A NOVEL CELL-CELL FUSION APPROACH COMBINED WITH IDENTIFICATION OF HOST FACTORS THAT INTERACT WITH THE ENV CT. TOGETHER, THE WORK OUTLINED HERE WILL EXPAND UPON A PRODUCTIVE LINE OF INVESTIGATION THAT SEEKS TO COMPREHENSIVELY DEFINE THE MECHANISM OF INCORPORATION OF ENV INTO HIV-1 PARTICLES.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $609.0k | 4/1/26 | ||
| Not listed | $609.0k | 4/14/25 | ||
| Not listed | $60.9k | 9/4/24 | ||
| Not listed | $60.9k | 9/4/24 | ||
| Not listed | $0 | 5/21/24 |