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. (J Allergy Clin Immunol 2015;136:81-6.)