Innate Immunity and Respiratory Syncytial Virus (RSV) Infection in Children (IIRI)
In this project we will study the capacity for single nucleotide polymorphisms (SNP) in TLR4 gene to induce varying levels of inflammatory chemokine and cytokine production.
Respiratory Syncytial Virus Infection
|Study Design:||Observational Model: Case Control
Time Perspective: Prospective
|Official Title:||Innate Immunity and RSV Infection in Children|
- Nasal Interferon (IFN)-a2 [ Time Frame: 1-5 days during acute illness (not after day 5 of illness) ] [ Designated as safety issue: No ]Interferon a2 was measured from nasal lavage samples by Luminex multiplex assay.
- Percentage of Participants With Detected Nasal Interferon (IL)-2 Cytokine Expression [ Time Frame: 1-5 days during acute illness (not after day 5 of illness) ] [ Designated as safety issue: No ]IL-2 measured from nasal lavage samples by Luminex multiplex assay
Biospecimen Retention: Samples With DNA
Nasal samples Supernatant from Peripheral mononuclear cell stimulation cultures DNA
|Study Start Date:||November 2003|
|Study Completion Date:||June 2008|
|Primary Completion Date:||May 2008 (Final data collection date for primary outcome measure)|
Toll-like Receptor 4 -2026/GG Genotype
Toll-like Receptor 4 (TLR4) -2026/GG Genotype of interest hypothesized to be associated with less inflammation during Respiratory Syncytial virus (RSV) infection
Toll-like Receptor 4 -2026/AG and AA Genotypes
Toll-like Receptor 4 (TLR4) -2026/AG and AA control genotypes hypothesized to be associated with more inflammation during respiratory syncytial virus (RSV) infection
Infection with RSV is the most common cause of respiratory tract illnesses (LRIs) in the first 3 years of life. There are significant social and health care costs associated with RSV-LRIs. More than 3% of US children are hospitalized each year due to RSV and 500 die annually. Several longitudinal studies have also suggested that children who have RSV-LRIs are at substantially increased risk of developing asthma in the first 3 years after infection and bronchial hyperresponsiveness (BHR) many years after the primary infection. Mechanisms involved in RSV disease are not well understood. Recent reports suggest that RSV may initiate the innate immune response through the pattern recognition receptor, Toll like receptor-4 (TLR4). In this project we will study the capacity for single nucleotide polymorphisms (SNP) in TLR4 gene to induce varying levels of inflammatory chemokine and cytokine production. It has been suggested that such a mechanism may result in altered immune responses to RSV infection and different clinical outcomes. This research has direct application to improving our understanding of bronchiolitis in early childhood, particularly those factors that influence severity of the disease, and may have implications for possible therapy of patients with bronchiolitis in the future.
|United States, Wisconsin|
|University of Wisconsin-Madison|
|Madison, Wisconsin, United States, 53792-9988|
|Principal Investigator:||Theresa W. Guilbert, MD||University of Wisconsin, Madison|