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Investigating the antiviral effects of CD43 and PSGL-1 on HIV-1 in cell-free infection and cell-to-cell transmission

Award Number: F31AI203399
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 02/01/2027
PERIOD OF PERFORMANCE END DATE: 01/31/2028

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Investigating the antiviral effects of CD43 and PSGL-1 on HIV-1 in cell-free infection and cell-to-cell transmission - Project Abstract Antiretroviral therapy (ART) for HIV-1 has decreased AIDS-related deaths and increased the quality of life for people living with HIV-1 (PLWH), but the emergence of drug-resistant HIV-1, HIV-1 latency, and side effects of some antiretroviral drugs are all key issues surrounding current treatments. Therefore, we are in constant need of investigating potential new targets for antiretrovirals in the HIV-1 life cycle. CD4+ T cells are the primary host for productive HIV-1 infection. Following the assembly of progeny HIV-1 particles, HIV-1 transmits to uninfected CD4+ T cells through both cell-free infection and cell-to-cell transmission. Of note, during HIV-1 assembly, virus particles incorporate large, sialylated, T cell-encoded transmembrane proteins such as CD43 and PSGL-1 into its viral envelope, which have been shown to suppress virus attachment to cells. Interestingly, sialylation has been reported to be altered in chronic infection possibly affecting the glycan structures of CD43 and PSGL-1. This application details experiments to address major knowledge gaps related to inhibitory effects of CD43 and PSGL-1 on HIV-1 attachment. One major question is whether the mechanism of inhibition of HIV-1 attachment to host cells by CD43 and PSGL-1 is electrostatic repulsion or steric hinderance. Another major question is how HIV-1 transmits to uninfected T cells successfully despite the presence of CD43 and PSGL-1 on the surface of virus-producing T cells. My central hypothesis is that sialic acid on CD43 and PSGL-1 is the main molecular determinant for the inhibition of HIV-1 attachment by these proteins and that cell-to-cell transmission is able to circumvent this effect. In Aim 1, I will examine the sialylation status of CD43 and PSGL-1 in transfected cells. In addition, I will use an enzymatic approach to examine the role played by sialic acid on virus-incorporated CD43 and PSGL-1 in its antiviral function. In Aim 2, I will use expansion microscopy, a super-resolution microscopy technique, to determine the nanoscale distribution of CD43 and PSGL-1 on infected, donor T cells at the virological synapse. In addition, I will check the sialylation status of the proteins at the virological synapse through fluorescent lectin staining and expansion microscopy. My proposed experiments will identify the molecular determinants for the inhibitory effects of CD43 and PSGL-1 on HIV-1 attachment and the role of CD43 and PSGL-1 in cell-to-cell transmission of HIV-1. Overall, this project will provide insight into the role of glycans on cell-free infection and cell-to-cell transmission of viruses.


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 = $50,114 )
2026	2026	REGENTS OF THE UNIVERSITY OF MICHIGAN	1109 GEDDES AVE STE 3300	ANN ARBOR	MI	48109	WASHTENAW	USA	Allergy and Infectious Diseases Research	000	1	8/1/2026	NEW	$50,114
														Subtotal = $50,114

Grand Total All Awards = $50,114

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Investigating the antiviral effects of CD43 and PSGL-1 on HIV-1 in cell-free infection and cell-to-cell transmission

Award Number: F31AI203399

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 02/01/2027

PERIOD OF PERFORMANCE END DATE: 01/31/2028

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