Genetic predisposition of RSV infection-related respiratory morbidity in preterm infants

The aim of this study was to assess whether prematurely born infants have a genetic predisposition to respiratory syncytial virus (RSV) infection-related respiratory morbidity. One hundred and forty-six infants born at less than 36 weeks of gestation were prospectively followed. Nasopharygeal aspira...

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Veröffentlicht in:European journal of pediatrics 2014-07, Vol.173 (7), p.905-912
Hauptverfasser: Drysdale, Simon B., Prendergast, Michael, Alcazar, Mireia, Wilson, Theresa, Smith, Melvyn, Zuckerman, Mark, Broughton, Simon, Rafferty, Gerrard F., Johnston, Sebastian L., Hodemaekers, Hennie M., Janssen, Riny, Bont, Louis, Greenough, Anne
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Sprache:eng
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Zusammenfassung:The aim of this study was to assess whether prematurely born infants have a genetic predisposition to respiratory syncytial virus (RSV) infection-related respiratory morbidity. One hundred and forty-six infants born at less than 36 weeks of gestation were prospectively followed. Nasopharygeal aspirates were obtained on every occasion the infants had a lower respiratory tract infection (LRTI) regardless of need for admission. DNA was tested for 11 single-nucleotide polymorphisms (SNPs). Chronic respiratory morbidity was assessed using respiratory health-related questionnaires, parent-completed diary cards at a corrected age of 1 year and review of hospital notes. Lung function was measured at a post menstrual age (PMA) of 36 weeks and corrected age of 1 year. A SNP in ADAM33 was associated with an increased risk of developing RSV LRTIs, but not with significant differences in 36-week PMA lung function results. SNPs in several genes were associated with increased chronic respiratory morbidity (interleukin 10 (IL10), nitric oxide synthase 2A (NOS2A), surfactant protein C (SFTPC), matrix metalloproteinase 16 (MMP16) and vitamin D receptor (VDR)) and reduced lung function at 1 year (MMP16, NOS2A, SFTPC and VDR) in infants who had had RSV LRTIs. Conclusions : Our results suggest that prematurely born infants may have a genetic predisposition to RSV LRTIs and subsequent respiratory morbidity which is independent of premorbid lung function.
ISSN:0340-6199
1432-1076
DOI:10.1007/s00431-014-2263-0