# Viral reactivation from ganglia in subarachnoid hemorrhage

> **NIH NIH R03** · UNIVERSITY OF WASHINGTON · 2020 · $77,750

## Abstract

Project Summary
Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease frequently leading
to death or poor functional outcome. A major complication of aSAH is the development of
cerebral vasospasm, which is defined as narrowing of the large and medium-sized
intracranial arteries. Between 30-70% of patients develop vasospasm after aSAH and half
of these may develop symptomatic delayed cerebral ischemia (DCI) with the incidence
peaking in the second week after ictus. Despite improvements in the clinical management
of aSAH over the last decade, DCI remains the single most important cause of morbidity
and mortality in those patients who survive the initial hemorrhage.
Limited information exists regarding underlying anatomic mechanisms of vasospasm in
aSAH. Cerebral blood vessels on the surface of the brain are surrounded by nerve fibers
that originate from sensory and autonomic nerve ganglia that are highly sensitive to
sympathetic nervous system activity. Elevated levels of catecholamines have been well
documented in aSAH, and in the acute setting, activation of perivascular sympathetic
nerves leads to an increase in vascular tone and as a result, decreases brain perfusion.
Paroxysmal cerebral vasospasm outside the acute setting suggests a different or delayed
mechanism perhaps through the same anatomic pathway.
We propose that herpesvirus reactivation in response to adrenergic activation of head and
neck ganglia during aSAH will be directly related and thus temporally correlated with the
occurrence of cerebral vasospasm. Given the shared anatomic pathways between glands,
viscera and cerebral blood vessels, we propose that non-invasive, simultaneous
monitoring of vascular tone and viral shedding from glandular secretions could
demonstrate a correlation between viral reactivation and vasospasm after aSAH. If correct,
antiviral agents would have the potential to reduce or prevent DCI in individuals with aSAH
and analysis of oral and ocular secretions after acute aSAH may provide a simple and
non-invasive predictive biomarker to assess risk of developing vasospasm.

## Key facts

- **NIH application ID:** 10107017
- **Project number:** 1R03NS120051-01
- **Recipient organization:** UNIVERSITY OF WASHINGTON
- **Principal Investigator:** Melanie Walker
- **Activity code:** R03 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $77,750
- **Award type:** 1
- **Project period:** 2020-09-01 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10107017

## Citation

> US National Institutes of Health, RePORTER application 10107017, Viral reactivation from ganglia in subarachnoid hemorrhage (1R03NS120051-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10107017. Licensed CC0.

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