# Receptor Usage and Regulation of the Immune Response in HSV Infection

> **NIH NIH R21** · NORTHWESTERN UNIVERSITY · 2024 · $194,748

## Abstract

Project Description:
Herpes simplex virus type I (HSV-1) infection is often asymptomatic or may produce recurrent lesions in and
around the mouth, commonly called “cold sores.” Ocular herpetic disease, typically caused by HSV-1 either
through primary infection or reactivation from the trigeminal ganglia (TG), can have serious sequelae, including
permanent corneal scarring and blindness. Herpes stromal keratitis (HSK) is one of the most common causes
of infectious blindness in the developed world, and worldwide produces over 40,000 new cases of severe
vision impairment or blindness each year. Interestingly, the majority of HSK tissue damage is thought to be
immune-mediated rather than resulting from direct lytic effects of the virus. Even after the virus has
successfully been cleared, high levels of inflammatory cytokines and chemokines, immune cell infiltrates, and
neovascularization persist. How HSV-1 infection of the eye leads to this chronic inflammatory syndrome is not
well understood. By studying cellular factors that influence the host immune response, we will delineate the
cascade of events that begin with a viral infection and end with chronic inflammation and vision loss. This
proposal represents a continuation of our studies examining cellular factors that are important for HSK using a
murine model. The studies proposed here will address the immunomodulatory functions of PILRA and HVEM
in Herpes Simplex Virus (HSV) Keratitis. By investigating how PILRA and HVEM contributes to HSK, we will
better understand the viral-host interactions inflammatory syndrome that persists in the absence of replicating
virus, providing a basis for therapeutic interventions for HSK.

## Key facts

- **NIH application ID:** 10908709
- **Project number:** 5R21AI173600-02
- **Recipient organization:** NORTHWESTERN UNIVERSITY
- **Principal Investigator:** Richard M Longnecker
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $194,748
- **Award type:** 5
- **Project period:** 2023-08-16 → 2026-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10908709

## Citation

> US National Institutes of Health, RePORTER application 10908709, Receptor Usage and Regulation of the Immune Response in HSV Infection (5R21AI173600-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10908709. Licensed CC0.

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