Early-life respiratory viral infections, atopic sensitization, and risk of subsequent development of persistent asthma
Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma. The nature of potential interactions between these risk factors was the subject of this study. A community-based cohort of 198 children at high atopic risk was followed fr...
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| Published in | Journal of allergy and clinical immunology Vol. 119; no. 5; pp. 1105 - 1110 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Mosby, Inc
01.05.2007
Elsevier Elsevier Limited American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1085-8725 1097-6825 1097-6825 |
| DOI | 10.1016/j.jaci.2006.12.669 |
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| Abstract | Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.
The nature of potential interactions between these risk factors was the subject of this study.
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.
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.
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.
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. |
|---|---|
| AbstractList | Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.
The nature of potential interactions between these risk factors was the subject of this study.
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.
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.
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.
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. Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma. The nature of potential interactions between these risk factors was the subject of this study. 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. 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. 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. 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. 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. 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. 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. Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.BACKGROUNDSevere lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.The nature of potential interactions between these risk factors was the subject of this study.OBJECTIVEThe nature of potential interactions between these risk factors was the subject of this study.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.METHODSA 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.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.RESULTSA 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.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.CONCLUSIONThese 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.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.CLINICAL IMPLICATIONSProtection 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. Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.The nature of potential interactions between these risk factors was the subject of this study.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.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.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.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. |
| Author | de Klerk, Nicholas H. Holt, Patrick G. Kusel, Merci M.H. Vohma, Vaike Johnston, Sebastian L. Sly, Peter D. Kebadze, Tatiana |
| AuthorAffiliation | b National Heart and Lung Institute, Imperial College, London a From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia |
| AuthorAffiliation_xml | – name: a From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia – name: b National Heart and Lung Institute, Imperial College, London |
| Author_xml | – sequence: 1 givenname: Merci M.H. surname: Kusel fullname: Kusel, Merci M.H. email: mercik@ichr.uwa.edu.au organization: From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia – sequence: 2 givenname: Nicholas H. surname: de Klerk fullname: de Klerk, Nicholas H. organization: From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia – sequence: 3 givenname: Tatiana surname: Kebadze fullname: Kebadze, Tatiana organization: National Heart and Lung Institute, Imperial College, London – sequence: 4 givenname: Vaike surname: Vohma fullname: Vohma, Vaike organization: From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia – sequence: 5 givenname: Patrick G. surname: Holt fullname: Holt, Patrick G. organization: From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia – sequence: 6 givenname: Sebastian L. surname: Johnston fullname: Johnston, Sebastian L. organization: National Heart and Lung Institute, Imperial College, London – sequence: 7 givenname: Peter D. surname: Sly fullname: Sly, Peter D. organization: From the Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18772458$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17353039$$D View this record in MEDLINE/PubMed |
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| Snippet | Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.
The nature of potential... Background Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma. Objective The... Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma. The nature of potential... Background Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma. Objective The... Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.The nature of potential... Background: Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma. Objective: The... Severe lower respiratory infections (LRIs) and atopic sensitization have been identified as independent risk factors for asthma.BACKGROUNDSevere lower... |
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| SubjectTerms | Acute respiratory infections Age Allergy and Immunology Asthma Asthma - epidemiology Asthma - etiology Biological and medical sciences Child, Preschool childhood asthma Children & youth Female Fever Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Hypersensitivity - complications Hypersensitivity - epidemiology Immunopathology Infant Influenza Male Medical sciences persistent wheeze Population Respiratory diseases Respiratory syncytial virus Respiratory Tract Infections - virology Rhinovirus Risk Factors RSV Viral infections Virus Diseases - complications Viruses |
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| Title | Early-life respiratory viral infections, atopic sensitization, and risk of subsequent development of persistent asthma |
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