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Unleashing the anti-HIV activity of lymphoid-resident NK cells

Award Number: F30AI203579
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 08/14/2026
PERIOD OF PERFORMANCE END DATE: 08/13/2030

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Unleashing the anti-HIV activity of lymphoid-resident NK cells - Project Summary Although HIV treatment regimens continue to advance, there has yet to be a broadly applicable cure for the 40 million people living with HIV (PLWH) globally. HIV’s ability to establish and maintain tissue and cellular reservoirs allows viral rebound during treatment interruptions and is the principal barrier to cure. The germinal centers (GCs) found within lymphoid tissues are known to be a critical site of HIV persistence, which is thought to be mediated by the exclusion of key immune effector cell types such as CD8 T cells and NK cells (NKCs) from the GC. In primates that are natural hosts of SIV and do not develop immunodeficiencies, highly active NKCs penetrate the GC and are thought to control the viral replication and prevent disease progression. Previous studies and our preliminary data have demonstrated increased penetration of these immune effectors into GCs during HIV infection, which raises the question how is HIV escaping elimination in this key sanctuary site? HLA-E signaling through its ligand NKG2A is known to disrupt NK dysfunction peripherally, and it has been implicated in GC CD8 T cell exhaustion in HIV but the role of this pathway in GC NKCs remains undefined. The proposed study aims to understand the role of this NKC signaling cascade in HIV persistence if modulation of this pathway or use of other immunostimulatory treatments can increase HIV control. We hypothesize that HIV’s effect of increasing HLA-E expression disrupts NKG2A signaling pathways and leads to a reversible dysfunction in GC NKCs. First, we will evaluate the presence, phenotype, and NKG2A signaling status of GC NKCs using access to rare HIV lymphoid tissues. This will be accomplished through microscopy techniques such as immunohistochemistry and immunofluorescence, and through single cell RNA sequencing. Leveraging our immune organoid model will allow for functional analysis of HLA-E-NKG2A signaling blockade and interrogation of this pathway’s role in acute HIV infection. Aim two will use the organoid model focus on whether immunostimulatory therapeutics can increase HIV reservoir clearance or disrupt establishment of infection. The expected outcomes include a deeper understanding of a key NKC regulatory signaling cascade in a critical HIV sanctuary site and whether existing immunotherapies demonstrate efficacy at reducing HIV burden in a tissue organoid model. These outcomes will identify potential mechanisms for reducing HIV reservoir size and inform HIV cure strategies.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $47,387 )
2026	2026	UNIVERSITY OF SOUTH FLORIDA	4202 E FOWLER AVE	TAMPA	FL	33620	HILLSBOROUGH	USA	Allergy and Infectious Diseases Research	000	1	8/4/2026	NEW	$47,387
2026	2026	UNIVERSITY OF SOUTH FLORIDA	4202 E FOWLER AVE	TAMPA	FL	33620	HILLSBOROUGH	USA	Allergy and Infectious Diseases Research	001	1	8/4/2026	NEW	$0
														Subtotal = $47,387

Grand Total All Awards = $47,387

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Unleashing the anti-HIV activity of lymphoid-resident NK cells

Award Number: F30AI203579

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 08/14/2026

PERIOD OF PERFORMANCE END DATE: 08/13/2030

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