alexa Viral Specific Factors Contribute to Clinical Respiratory Syncytial Virus Disease Severity Differences in Infants
ISSN: 2327-5073

Clinical Microbiology: Open Access
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Research Article

Viral Specific Factors Contribute to Clinical Respiratory Syncytial Virus Disease Severity Differences in Infants

Tonya M Thompson1,5#, Philippa L Roddam1,3,4#, Lisa M Harrison1,3,4, Jody A Aitken1,3,4, and John P DeVincenzo1,2,3,4*

1University of Tennessee School of Medicine, Department of Pediatrics

2University of Tennessee Graduate School of Health Sciences, Department of Molecular Sciences

3Le Bonheur Children’s Hospital

4The Children’s Foundation Research Institute at Le Bonheur Children’s Hospital, Memphis, TN 38103

5University of Arkansas for Medical Sciences, Department of Pediatric Emergency Medicine, Little Rock, AR 72202

#Authors contributed equally

*Corresponding Author:
John P DeVincenzo
CFRI Research Tower, Room 433, UTHSC
Le Bonheur Children’s Hospital, 50 North Dunlap Street
Memphis, TN 38103, USA
Tel: 901-287-5377
Fax: 901-287-4478
E-mail: [email protected]

Received date: March 04, 2015; Accepted date: June 25, 2015; Published date: June 29, 2015

Citation: Thompson TM, Roddam PL, Harrison LM, Aitken JA, DeVincenzo JP (2015) Viral Specific Factors Contribute to Clinical Respiratory Syncytial Virus Disease Severity Differences in Infants. Clin Microbiol 4:206. doi: 10.4172/2327-5073.1000206

Copyright: © 2015 Thompson TM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Background: There is a wide range of severity of respiratory syncytial viral (RSV) disease in previously healthy infants. Host factors have been well demonstrated to contribute to disease severity differences. However the possibility of disease severity differences being produced by factors intrinsic to the virus itself has rarely been studied. Methods: Low-passage isolates of RSV collected prospectively from infants with different degrees of RSV disease severity were evaluated in vitro, holding host factors constant, so as to assess whether isolates induced phenotypically different cytokine/chemokine concentrations in a human lung epithelial cell line. Sixty-seven RSV isolates from previously healthy infants (38 hospitalized for acute RSV infection (severe disease) and 29 never requiring hospitalization (mild disease)) were inoculated into A549, lung epithelial cells at precisely controlled, low multiplicity of infection to mimic natural infection. Cultures were evaluated at 48 hours, 60 hours, and 72 hours to evaluate area under the curve (AUC) cytokine/chemokine induction. Results: Cells infected with isolates from severely ill infants produced higher mean concentrations of all cytokine/ chemokines tested (IL-1α, IL-6, IL-8 and RANTES) at all-time points tested. RSV isolates collected from infants with severe disease induced significantly higher AUCIL-8 and AUCRANTES secretion in infected cultures than mild disease isolates (p=0.028 and p=0.019 respectively). IL-8 and RANTES concentrations were 4 times higher at 48 hours for these severely ill infant isolates. Additionally, 38 isolates were evaluated at all-time points for quantity of virus. RSV concentration significantly correlated with both IL-8 and RANTES at all-time points. Neither cytokine/ chemokine concentrations nor RSV concentrations were associated with RSV subgroup. Discussion: Infants' RSV disease severity differences may be due in part to intrinsic viral strain-specific characteristics.

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