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Early-life respiratory viral infections, atopic sensitization, and risk of subsequent development of persistent
Merci M H Kusel1, Nicholas H de Klerk, Tatiana Kebadze
1Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia, West Perth, Australia. mercik@ichr.uwa.edu.au
Insights
Infant viral infections and early atopic sensitization interact to significantly increase a child's risk for developing asthma by age five. Protecting high-risk infants from severe respiratory infections may be key for primary asthma prevention.
Area of Science:
- Pediatric Allergy and Immunology
- Respiratory Medicine
- Epidemiology
Background:
- Severe lower respiratory infections (LRIs) and atopic sensitization are independent asthma risk factors.
- Understanding the interplay between these factors is crucial for asthma prevention strategies.
Purpose of the Study:
- To investigate the interaction between severe LRIs and atopic sensitization in early childhood.
- To determine their combined effect on the development of asthma up to age five.
Main Methods:
- A community-based cohort study followed 198 high-atopy risk children from birth to 5 years.
- Recorded acute respiratory illnesses in the first year, collected viral samples, and assessed wheeze, asthma, and atopy at multiple time points.
Main Results:
- LRIs occurred in 33% of acute respiratory illnesses, with rhinoviruses and RSV being common.
- Early atopic sensitization (< or =2 years) combined with wheezy/febrile LRIs (especially RSV or rhinovirus) significantly increased asthma risk by age five.
- These associations were specific to children with early sensitization.
Conclusions:
- Viral infections and atopy interact in infancy to promote later asthma development.
- The co-occurrence of viral LRIs and atopy during a critical developmental window maximizes asthma risk.
- Interventions protecting high-risk infants from severe respiratory infections could be a primary asthma prevention strategy.
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 (< or =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.
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