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Association between respiratory infections in early life and later asthma is independent of virus type - 03/07/15

Doi : 10.1016/j.jaci.2015.02.024 
Klaus Bønnelykke, MD, PhD a, Nadja Hawwa Vissing, MD, PhD a, Astrid Sevelsted, MSci a, Sebastian L. Johnston, MD, PhD b, Hans Bisgaard, MD, DMSc a,
a Copenhagen Prospective Studies on Asthma in Childhood, Faculty of Health and Medical Sciences, University of Copenhagen & Danish Pediatric Asthma Center, Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark 
b Airway Disease Infection Section, MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, and Centre for Respiratory Infection, National Heart & Lung Institute, Imperial College London, London, United Kingdom 

Corresponding author: Hans Bisgaard, MD, DMSc, Copenhagen Prospective Studies on Asthma in Childhood, Faculty of Health and Medical Sciences, University of Copenhagen & Danish Pediatric Asthma Center, Gentofte Hospital, University of Copenhagen, Denmark Ledreborg Alle 34 DK-2820 Gentofte, Denmark.

Abstract

Background

Lower respiratory tract infections in the first years of life are associated with later asthma, and this observation has led to a focus on the potential causal role of specific respiratory viruses, such as rhinoviruses and respiratory syncytial virus, in asthma development. However, many respiratory viruses and bacteria trigger similar respiratory symptoms and it is possible that the important risk factors for asthma are the underlying susceptibility to infection and the exaggerated reaction to such triggers rather than the particular triggering agent.

Objective

We sought to study the association between specific infections in early life and development of asthma later in childhood.

Methods

Three hundred thirteen children were followed prospectively in the Copenhagen Prospective Studies of Asthma in Childhood2000 high-risk birth cohort. Nine respiratory virus types (respiratory syncytial virus, rhinoviruses, other picornaviruses, coronaviruses 229E and OC43, parainfluenza viruses 1-3, influenza viruses AH1, AH3, and B, human metapneumovirus, adenoviruses, and bocavirus) and 3 pathogenic airway bacteria (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis) were identified in airway secretions sampled during episodes of troublesome lung symptoms in the first 3 years of life. Asthma was determined by age 7 years.

Results

In unadjusted analyses, all viruses and pathogenic bacteria identified during episodes of troublesome lung symptoms were associated with increased risk of asthma by age 7 years with similar odds ratios for all viruses and pathogenic bacteria. After adjustment for the frequency of respiratory episodes, the particular triggers were no longer associated with asthma.

Conclusion

The number of respiratory episodes in the first years of life, but not the particular viral trigger, was associated with later asthma development. This suggests that future research should focus on the susceptibility and exaggerated response to lower respiratory tract infections in general rather than on the specific triggering agent.

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Key words : Child, asthma, virus, bacteria, respiratory tract infection

Abbreviations used : COPSAC, OR, RSV


Plan


 Data in this manuscript were published as an abstract at the European Academy of Allergy and Clinical Immunology Congress 2014 but not in any other format.
 Disclosure of potential conflict of interest: Copenhagen Prospective Studies on Asthma in Childhood (COPSAC) is funded by private and public research funds all listed on www.copsac.com. The Lundbeck Foundation (grant no. R16-A1694); the Ministry of Health (grant no. 903516); the Danish Council for Strategic Research (grant no. 0603-00280B); the Danish Council for Independent Research and the Capital Region Research Foundation have provided core support for COPSAC. Thermo Fischer Scientific Inc sponsored the IgE analyses. No pharmaceutical company was involved in the study. The funding agencies did not have any role in design and conduct of the study; collection, management, and interpretation of the data; or preparation, review, or approval of the manuscript. S. L. Johnston is supported by ERC FP7 Advanced grant 233015, a Chair from Asthma UK (CH11SJ), MRC Centre Grant G1000758, and Predicta FP7 Collaborative Project grant 260895. H. Bisgaard is employed by the Capital Region of Denmark, which has received funding from the Lundbeck Foundation and has received or has grants pending from the European Research Council, National Institutes of Health, and Novo Nordisk and has received compensation for providing expert testimony from the European Medicines Agency. The rest of the authors declare that they have no relevant conflicts of interest.


© 2015  American Academy of Allergy, Asthma & Immunology. Publié par Elsevier Masson SAS. Tous droits réservés.
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Vol 136 - N° 1

P. 81 - juillet 2015 Retour au numéro
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