# Neuropilin-1 is a putative entry receptor for murine cytomegalovirus

> **NIH NIH F31** · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 2020 · $26,500

## Abstract

Project Summary
Cytomegalovirus (CMV) is a leading cause of oral ulcerations in immunocompromised individuals and
is a factor in periodontal disease. There may also be a link between CMV infection and cleft lip/palate
development. Saliva is a major route of transmission for the virus. Infecting over half of the adult population
worldwide, CMV is consequently a major oral health concern. The broad tissue tropism of CMV is one reason
the virus causes severe illness in these tissues. However, much is still not understood about what dictates the
ability of the virus to enter various cell types. Entry receptors for a virus are a major determinant of viral
tropism. While much work has been done on CMV entry into fibroblasts, the identity of the entry receptor used
for infection of epithelial and endothelial cells has remained unknown until just in the last year Neuropilin-2 was
put forward. We have independently identified Neuropilin-1 (Nrp-1) as a putative entry receptor for murine CMV
(MCMV). No entry receptor for MCMV has been proposed before now. Using MCMV to study the details of
Nrp-1-dependent infection will provide insights into a key CMV-host interaction that may be targeted to block
infection and reduce infections in the mouth.
No role for Nrp-1 in MCMV infection has been reported previously. Preliminary data points to Nrp-1 as
mediating viral entry. This will first be investigated more closely by assessing colocalization of Nrp-1 and
MCMV during infection, measuring binding between virus and Nrp-1, and quantifying viral internalization in the
absence of Nrp-1. Next, the mode of entry regulated by Nrp-1 will be determined using inhibitors of endocytic
pathways and comparing markers of these pathways during infection with and without Nrp-1. Taking
advantage of MCMV as a natural mouse pathogen, we will also test whether Nrp-1 is required for infection and
spread to the salivary glands in vivo.
Lastly, the mechanics of the interaction between the virus and Nrp-1 will be examined. The viral protein
bound by Nrp-1 will be identified by immunoprecipitations and mass spectrometry. Additionally, the region of
Nrp-1 that binds to the virus will be located. Mutant Nrp-1 constructs will be generated and used to reconstitute
Nrp-1 knockout cells. The ability of each of these mutants to allow infection will then be determined. This
information will be critical for the design of a therapy that targets the receptor-binding activity of CMV.

## Key facts

- **NIH application ID:** 9989411
- **Project number:** 1F31DE029395-01A1
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
- **Principal Investigator:** REBECCA LANE
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $26,500
- **Award type:** 1
- **Project period:** 2020-04-01 → 2020-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9989411

## Citation

> US National Institutes of Health, RePORTER application 9989411, Neuropilin-1 is a putative entry receptor for murine cytomegalovirus (1F31DE029395-01A1). Retrieved via AI Analytics 2026-06-12 from https://api.ai-analytics.org/grant/nih/9989411. Licensed CC0.

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