# Neurogenic Inflammatory Response to RSV

> **NIH NIH R01** · TULANE UNIVERSITY OF LOUISIANA · 2022 · $510,376

## Abstract

PROJECT DESCRIPTION
Respiratory syncytial virus (RSV) is the most important respiratory pathogen in infancy and early childhood,
and strong epidemiologic evidence links this infection with subsequent wheezing and asthma. In the previous
funding cycle, we found that RSV is able to spread hematogenously across the placenta from the respiratory
tract of rat dams to their offspring. Prenatal RSV infection is associated with increased airway reactivity after
postnatal reinfection with RSV due to aberrant cholinergic innervation of the respiratory tract and enhanced
contractility of the airway smooth muscle. Furthermore, pups born to RSV-infected dams show selective
impairment of innate anti-viral immunity, with virtual suppression of key Th1-type cytokines like IFN- and IL-2.
These changes persist after secondary reinfection and might provide a plausible explanation to the
development of chronic airway dysfunction in children with history of severe RSV infections in infancy.
Recently, data reported by us and by other investigators have increased significantly the translational potential
of our preclinical studies, as there is growing evidence that RSV
crosses the uterine-placental interface
in
humans
and infects the fetal lungs
by vertical transmission. This evidence challenges the paradigm that
RSV infection is acquired only after birth and has shifted our attention to the prenatal effects of this virus, which
may result in more severe and lasting consequences by interfering with lung development during a critical
“window of opportunity”. The specific aims of the present proposal are organized around the evaluation of a
central hypothesis articulated in the following components: 1. RSV infection vertically transmitted through the
placenta from the infected mother to the fetus modifies expression and activity of key ion channels and
receptors in the developing lungs, predisposing to postnatal airway hyperreactivity; 2. Unhealthy environmental
conditions during pregnancy, such as unbalanced nutrition or exposure to particulate pollution, modulate
vertical transmission of RSV to the fetus, and may amplify its long-term consequences in terms of airway
hyperreactivity; and 3. In utero transmission of infective virus to the fetus occurs in humans, is associated with
adverse perinatal respiratory outcomes, and might lead to persistent airway dysfunction and asthma in
childhood.This research is likely to have a sustained and powerful impact because it will test the paradigm-
shifting hypothesis that common respiratory viruses modulate lung development in humans and predispose to
chronic respiratory pathology by infecting the fetus before birth. The proposed experiments are also designed
to provide critical information concerning the influence of environmental factors on fetal lung development and
the prenatal modulation of receptors essential to the control of airway function, and will correlate this
information to the development of persistent airway hyper...

## Key facts

- **NIH application ID:** 10433987
- **Project number:** 5R01HL061007-18
- **Recipient organization:** TULANE UNIVERSITY OF LOUISIANA
- **Principal Investigator:** Giovanni Piedimonte
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $510,376
- **Award type:** 5
- **Project period:** 1999-07-01 → 2025-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10433987

## Citation

> US National Institutes of Health, RePORTER application 10433987, Neurogenic Inflammatory Response to RSV (5R01HL061007-18). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10433987. Licensed CC0.

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