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Dissecting Neuroglial Innate Immunity in vivo against Polyomavirus CNS Infection

Award Number: F31NS139582
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 06/01/2025
PERIOD OF PERFORMANCE END DATE: 05/31/2028

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Dissecting Neuroglial Innate Immunity in vivo against Polyomavirus CNS Infection - PRORJECT ABSTRACT: JC Polyomavirus (JCPyV) is a ubiquitous asymptomatic virus that infects up to 90% of humans. In immunocompromised individuals, JCPyV can cause progressive multifocal leukoencephalopathy (PML), an often-lethal demyelinating neurodegenerative disease. Because polyomaviruses (PyV) are species-specific, mechanisms of PML pathogenesis are incompletely understood. The Lukacher group studies Mouse Polyomavirus (MuPyV), a natural murine virus, to define virologic and immunologic factors involved in PyV CNS infection and disease. Published work from the Lukacher group has shown that Type I Interferons (IFNs) directly inhibit MuPyV replication and are necessary to mitigate MuPyV encephalitis. The pathway(s) of Type I IFN induction during PyV infection in vivo is unknown. In vitro, cyclic GMP-AMP Synthase (cGAS) and Stimulator of IFN Genes (STING) have been implicated in limiting viral infections by a number of viruses with double-stranded (ds) genomes, including JCPyV and MuPyV. Our preliminary data using STING-/- cells confirms the importance of STING in inducing Type I IFN upon MuPyV infection in tissue culture. In this way, STING is the central adapter protein responsible for the first wave of Type I IFNs. Signal Transducer and Activator of Transcription (STAT) 1 is a downstream target of Type I IFNs. Signaling via STAT1 potently inhibits MuPyV replication. How STAT1 acts as a mediator of antiviral activity in MuPyV infected cells in vivo is unknown. The goal of this proposal is to determine whether cGAS-STING (Aim 1) and/or STAT1 (Aim 2) act in MuPyV-infected neuroglia in vivo to promote the antiviral Type I IFN axis and control virus- induced neurovirulence.


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 = $37,108 )
2026	2026	PENNSYLVANIA STATE UNIVERSITY	500 UNIVERSITY DRIVE	HERSHEY	PA	17033	DAUPHIN	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	2	6/5/2026	NON-COMPETING CONTINUATION	$37,108
														Subtotal = $37,108

Issue Date FY: 2025 ( Subtotal = $36,472 )
2025	2025	PENNSYLVANIA STATE UNIVERSITY	500 UNIVERSITY DRIVE	HERSHEY	PA	17033	DAUPHIN	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	001	1	5/7/2025	NEW	$0
2025	2025	PENNSYLVANIA STATE UNIVERSITY	500 UNIVERSITY DRIVE	HERSHEY	PA	17033	DAUPHIN	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	002	1	9/8/2025	NEW	$564
2025	2025	PENNSYLVANIA STATE UNIVERSITY	500 UNIVERSITY DRIVE	HERSHEY	PA	17033	DAUPHIN	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	5/7/2025	NEW	$35,908
														Subtotal = $36,472

Grand Total All Awards = $73,580

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Dissecting Neuroglial Innate Immunity in vivo against Polyomavirus CNS Infection

Award Number: F31NS139582

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 06/01/2025

PERIOD OF PERFORMANCE END DATE: 05/31/2028

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