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Glycosylation as a host defense strategy for multiple alphaviruses

Award Number: K99AI196249
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 05/06/2026
PERIOD OF PERFORMANCE END DATE: 04/30/2028

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Glycosylation as a host defense strategy for multiple alphaviruses - Project Summary To gain access to cells, most viruses attach to receptor molecules. While many virus receptors have been identified, the impact of post-translational modifications on receptor function remains understudied. Glycosylation is a major type of post-translational modification of cell surface proteins, and viruses often exploit cell surface glycans for entry. However, given the extreme heterogeneity of glycosylation, it is unlikely that all glycans play equivalent roles in host-virus interactions. This proposal posits that specific glycosylation patterns can disrupt virus-receptor interactions, serving as a host defense mechanism against viral entry. My preliminary studies identify β1,3-N-acetylglucosaminyltransferase 2 (B3GNT2) as an interferon-stimulated gene that strongly inhibits multiple alphaviruses, including Venezuelan equine encephalitis virus (VEEV). B3GNT2 catalyzes the biosynthesis of poly-N-acetyllactosamine (polyLacNAc) chains leading to heavy and bulky glycosylation of LDLRAD3, a host receptor for VEEV. Consistent with its role in receptor glycosylation, B3GNT2 reduces VEEV attachment to the cell surface. Based on these findings, I hypothesize that B3GNT2 inhibits VEEV entry by glycosylating the viral receptor and may protect against VEEV-induced pathogenesis in vivo. Given its broad antiviral effects against multiple alphaviruses, I further hypothesize that B3GNT2 inhibits other alphaviruses including Chikungunya virus (CHIKV), through a similar mechanism. In the K99 mentored phase, I will integrate biochemical, cell biological, and glycan-based approaches to define the antiviral mechanism of B3GNT2 against VEEV (Aim 1) and investigate its antiviral role in VEEV pathogenesis using mouse models (Aim 2). In the R00 phase, I will extend these studies to CHIKV infection in B3gnt2 knockout mice and define the role of polyLacNAc glycosylation in blocking receptor-mediated entry of multiple alphaviruses (Aim 3). These studies will provide key insight into how host cells prevent viral entry through glycosylation and establish experimental tools to explore the broader role of glycosylation in host-pathogen interactions.


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 = $149,035 )
2026	2026	THE UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER	5323 HARRY HINES BLVD	DALLAS	TX	75390	DALLAS	USA	Allergy and Infectious Diseases Research	000	1	5/7/2026	NEW	$149,035
														Subtotal = $149,035

Grand Total All Awards = $149,035

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Glycosylation as a host defense strategy for multiple alphaviruses

Award Number: K99AI196249

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 05/06/2026

PERIOD OF PERFORMANCE END DATE: 04/30/2028

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