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Mechanisms of Nuclear Egress in Gamma-herpesviruses

Award Number: F31AI191719
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/27/2026
PERIOD OF PERFORMANCE END DATE: 09/26/2027

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Mechanisms of Nuclear Egress in Gamma-herpesviruses - PROJECT SUMMARY/ABSTRACT Kaposi’s sarcoma-associated herpesvirus (KSHV) is an enveloped, double-stranded-DNA g-herpesvirus and class I carcinogen. KSHV is the causative agent of Kaposi’s sarcoma, primary effusion lymphomas, and multicentric Castleman’s disease. In sub-Saharan Africa, it has seroprevalence rates as high as 80% and causes endemic disease. The effectiveness of this oncogenic virus is largely attributed to its ability to reactivate at opportune times. During lytic infection, KSHV – like all herpesviruses – translocates newly assembled capsids from the nucleus into the cytoplasm for maturation into infectious virions. To accomplish this, KSHV utilizes an unusual process termed “nuclear egress,” in which viral capsids exit the nucleus by undergoing nuclear membrane budding and fusion events. The nuclear egress complex (NEC) is a conserved, virally encoded heterodimer that is required for nuclear egress and can bud membranes independently. Prior work from distantly related neurotropic a- herpesviruses demonstrated that the NEC promotes budding by oligomerizing into hexagonal, membrane-bound coats. However, recent studies suggested that the oncogenic g-herpesviruses KSHV and EBV may have structurally and functionally distinct NECs. Therefore, I hypothesize the KSHV NEC has a distinct membrane remodeling mechanism to support nuclear egress. The objective of this proposal is to characterize the mechanisms by which KSHV NEC remodels nuclear membranes to mediate nuclear egress. In Aim 1, I will characterize KSHV NEC function in vivo and visualize nuclear egress and nuclear membrane remodeling events in KSHV infected cells using TEM and cryo-electron tomography. In Aim 2, I will use x-ray crystallography, cryo-EM/ET, and structure-guided mutagenesis to determine the geometry of KSHV NEC coats and the role their formation plays in membrane budding and nuclear egress. This proposal is innovative as it will use cutting-edge approaches to yield new mechanistic insights into the process of nuclear egress in g-herpesviruses. It is significant as it will identify key functional regions within the KSHV NEC to inform the development of anti-KSHV therapeutics designed to block nuclear egress. This proposal has the potential to make major contributions for the development of therapeutics against KSHV and its associated cancers. My sponsor, Dr. Ekaterina Heldwein, will ensure that I acquire the technical and conceptual skills necessary for the successful completion of this project and for my development into a premier scientist so that I may achieve my long-term career goal of running my own virology lab.


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 = $45,726 )
2026	2026	TRUSTEES OF TUFTS COLLEGE	136 HARRISON AVE	BOSTON	MA	02111	SUFFOLK	USA	Allergy and Infectious Diseases Research	000	1	3/27/2026	NEW	$45,726
														Subtotal = $45,726

Grand Total All Awards = $45,726

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Mechanisms of Nuclear Egress in Gamma-herpesviruses

Award Number: F31AI191719

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/27/2026

PERIOD OF PERFORMANCE END DATE: 09/26/2027

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