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Role of FOXK subfamily in KSHV infection

Award Number: F31DE034303
ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 08/16/2024
PERIOD OF PERFORMANCE END DATE: 08/15/2027

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Role of FOXK subfamily in KSHV infection - Project Summary Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus with a biphasic lifecycle associated with several diseases such as Kaposi's sarcoma and primary effusion lymphoma (PEL). It is primarily spread through saliva making the oral cavity a critical site for initial infection. KSHV encodes an immediate early virion-associated tegument protein that is vital for efficient lytic reactivation and virus production. Following up on a proteomics study of KSHV factors in uninfected cells, our coimmunoprecipitation and imaging analysis in primary effusion lymphoma (PEL) cells during lytic reactivation of KSHV demonstrated that an immediate early protein of KSHV interacts with host transcription factors, FOXK1 and FOXK2. FOXK1 and FOXK2 belong to the Forkhead family of transcription factors. FOXK1 and FOXK2 are unique as they are the only Forkhead proteins which carry a Forkhead-associated (FHA) domain. FOXK proteins are ubiquitously expressed and play a key role in cellular processes such as cell cycle regulation, cancer development, and autophagy regulation. Their role in KSHV infection is not well understood though. Preliminary data from this proposal supports a pro-viral role for these host transcription factors during KSHV's lytic cycle. The purpose of this project is to dissect the importance of the interaction between the immediate early KSHV tegument protein and FOXK proteins and identify novel targets genome-wide of the immediate early KSHV tegument protein during reactivation and de novo infection. A combination of genome-wide studies coupled with KSHV mutants will be used to analyze how the FOXK and immediate early tegument proteins affects KSHV infection. In summary, I predict that this novel host-pathogen interaction might be engaged by KSHV, in order to promote its lytic cycle in the oral cavity and beyond, thus by understanding the mechanism, we could uncover future therapeutic targets. The completion of this project will provide in-depth training in epigenetics, virology and genomics approaches. These skills will be enhanced in the outstanding research environment provided by the Oral Biology department at the University of Florida College of Dentistry.


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: 2025 ( Subtotal = $46,667 )
2025	2025	UNIVERSITY OF FLORIDA	1523 UNION RD RM 207	GAINESVILLE	FL	32611	ALACHUA	USA	Oral Diseases and Disorders Research	000	2	7/28/2025	NON-COMPETING CONTINUATION	$46,667
														Subtotal = $46,667

Issue Date FY: 2024 ( Subtotal = $44,982 )
2024	2024	UNIVERSITY OF FLORIDA	1523 UNION RD RM 207	GAINESVILLE	FL	32611	ALACHUA	USA	Oral Diseases and Disorders Research	001	1	7/22/2024	NEW	$0
2024	2024	UNIVERSITY OF FLORIDA	1523 UNION RD RM 207	GAINESVILLE	FL	32611	ALACHUA	USA	Oral Diseases and Disorders Research	000	1	7/22/2024	NEW	$44,982
														Subtotal = $44,982

Grand Total All Awards = $91,649

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Role of FOXK subfamily in KSHV infection

Award Number: F31DE034303

ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 08/16/2024

PERIOD OF PERFORMANCE END DATE: 08/15/2027

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