The Journal of Allergy and Clinical Immunology
Volume 119, Issue 5 , Pages 1105-1110, May 2007

Early-life respiratory viral infections, atopic sensitization, and risk of subsequent development of persistent asthma

  • Merci M.H. Kusel, MBBS, PhD

      Affiliations

    • From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia
    • Corresponding Author InformationReprint requests: Merci M. H. Kusel, MBBS, PhD, Senior Research Officer, Division of Clinical Sciences, Telethon Institute for Child Health Research, P.O. Box 855, West Perth 6872, Australia.
  • ,
  • Nicholas H. de Klerk, MSc, PhD

      Affiliations

    • From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia
  • ,
  • Tatiana Kebadze, MD

      Affiliations

    • National Heart and Lung Institute, Imperial College, London
  • ,
  • Vaike Vohma, BSc(Hons)

      Affiliations

    • From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia
  • ,
  • Patrick G. Holt, DSc

      Affiliations

    • From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia
  • ,
  • Sebastian L. Johnston, MD, PhD, FRCP

      Affiliations

    • National Heart and Lung Institute, Imperial College, London
  • ,
  • Peter D. Sly, MD, FRACP, DSc

      Affiliations

    • From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia

Received 6 September 2006; received in revised form 5 December 2006; accepted 11 December 2006. published online 15 March 2007.

Perth, Australia, and London, United Kingdom

Background

Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.

Objective

The nature of potential interactions between these risk factors was the subject of this study.

Methods

A community-based cohort of 198 children at high atopic risk was followed from birth to 5 years. All episodes of acute respiratory illness in the first year were recorded and postnasal aspirates were collected for viral identification. History of wheeze and asthma was collected annually, and atopy was assessed at 6 months, 2 years, and 5 years.

Results

A total of 815 episodes of acute respiratory illness were reported, and 33% were LRIs. Viruses were detected in 69% of aspirates, most commonly rhinoviruses (48.3%) and respiratory syncytial virus (10.9%). At 5 years, 28.3%(n = 56) had current wheeze, and this was associated with wheezy [odds ratio (OR), 3.4 (1.2-9.7); P = .02] and/or febrile LRI [OR, 3.9 (1.4-10.5); P = .007], in particular those caused by respiratory syncytial virus or rhinoviruses [OR, 4.1 (1.3-12.6); P = .02]. Comparable findings were made for current asthma. Strikingly these associations were restricted to children who displayed early sensitization (≤2 years old) and not observed in nonatopic patients or those sensitized later.

Conclusion

These data suggest viral infections interact with atopy in infancy to promote later asthma. Notably the occurrence of both of these events during this narrow developmental window is associated with maximal risk for subsequent asthma, which suggests a contribution from both classes of inflammatory insults to disease pathogenesis.

Clinical implications

Protection of “high-risk” children against the effects of severe respiratory infections during infancy may represent an effective strategy for primary asthma prevention. The potential benefits of these strategies merit more careful evaluation in this age group.

Key words: Acute respiratory infections, childhood asthma, persistent wheeze, rhinovirus, RSV

Abbreviations used: ARI, Acute respiratory illness, LRI, Lower respiratory illness, NPA, Nasopharyngeal aspirate, OR, Odds ratio, RSV, Respiratory syncytial virus, SPT, Skin prick test, wLRI, Wheezy lower respiratory tract illness

 

 Supported by a National Health and Medical Research Council (Australia) Grant, the British Lung Foundation/Severin Wunderman, and the Family Foundation Programme Grant P00/2.Disclosure of potential conflict of interest: The authors have declared that they have no conflict of interest.

PII: S0091-6749(07)00238-2

doi:10.1016/j.jaci.2006.12.669

The Journal of Allergy and Clinical Immunology
Volume 119, Issue 5 , Pages 1105-1110, May 2007