Thursday, January 8, 2026 1/8/2026

Interplay between nuclear stress responses and herpesvirus latency

Award Number: R01AI176335
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 11/08/2023
PERIOD OF PERFORMANCE END DATE: 10/31/2028

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Interplay between nuclear stress responses and herpesvirus latency - SUMMARY Neurotrophic a-herpesvirus including herpes simplex virus-1 (HSV1) establish lifelong, latent (non-replicating) infections in sensory and sympathetic neurons. Recurring reactivation episodes triggered in response to physiological stress interrupt latency and allow virus reproduction, shedding and spread to new hosts. While it has long been known that HSV1 reactivation can be triggered by a perplexing variety of physiological and neurological stresses, the underlying molecular mechanisms have remained obscure. Recent studies using cultured primary neurons to model HSV1 latency and reactivation, allows us to build a detailed but still incomplete picture of how the virus is maintained in a dormant state and how stress response pathways converge to disrupt this control leading to reactivation. By applying cutting-edge single cell technologies to a well-defined primary neuron infection model, we have now identified neuronal factors that are rapidly mobilized in response to HSV1 reactivation and have the potential to block the virus replication program at a defined stage. The long-reaching goal of this project is to elucidate the molecular mechanisms responsible for this cell-intrinsic host response. We propose studies to identify the viral reactivation signature recognized by the host neuron and will determine why virus gene expression is selectively inhibited. Furthermore, our multifaceted approach will allow us to decipher the complex relationship between a viral parasite and its human host. By defining the molecular processes involved in regulating the behavior of latent virus we hope to gain a better understanding how neurons can be protected from a wide range of intrinsic and extrinsic insults.


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 = $677,273 )
2026	2026	NEW YORK UNIVERSITY	550 1ST AVE	NEW YORK	NY	10016	NEW YORK	USA	Allergy and Infectious Diseases Research	000	3	12/5/2025	NON-COMPETING CONTINUATION	$677,273
														Subtotal = $677,273

Issue Date FY: 2025 ( Subtotal = $656,955 )
2025	2025	NEW YORK UNIVERSITY	550 1ST AVE	NEW YORK	NY	10016	NEW YORK	USA	Allergy and Infectious Diseases Research	000	2	11/1/2024	NON-COMPETING CONTINUATION	$656,955
														Subtotal = $656,955

Issue Date FY: 2024 ( Subtotal = $673,035 )
2024	2024	NEW YORK UNIVERSITY	550 1ST AVE	NEW YORK	NY	10016	NEW YORK	USA	Allergy and Infectious Diseases Research	001	1	3/14/2024	NEW	$0
2024	2024	NEW YORK UNIVERSITY	550 1ST AVE	NEW YORK	NY	10016	NEW YORK	USA	Allergy and Infectious Diseases Research	000	1	11/8/2023	NEW	$605,732
2024	2024	NEW YORK UNIVERSITY	550 1ST AVE	NEW YORK	NY	10016	NEW YORK	USA	Allergy and Infectious Diseases Research	002	1	9/3/2024	NEW	$67,303
														Subtotal = $673,035

Grand Total All Awards = $2,007,263

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Interplay between nuclear stress responses and herpesvirus latency

Award Number: R01AI176335

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 11/08/2023

PERIOD OF PERFORMANCE END DATE: 10/31/2028

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