Early-life respiratory infections and asthma development: Role in disease pathogenesis and potential targets for disease prevention

Avraham Beigelman*, Leonard B. Bacharier

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

72 Scopus citations

Abstract

Purpose of review This article presents recent findings and perspectives on the relationship between early-life respiratory infections and asthma inception, and discusses emerging concepts on strategies that target these infectious agents for asthma prevention. Recent findings Cumulative evidence supports the role of early-life viral infections, especially respiratory syncytial virus and human rhinovirus, as major antecedents of childhood asthma. These viruses may have different mechanistic roles in the pathogenesis of asthma. The airway microbiome and virus-bacteria interactions in early life have emerged as additional determinants of childhood asthma. Innovative strategies for the prevention of these early-life infections, or for attenuation of acute infection severity, are being investigated and may identify effective strategies for the primary and secondary prevention of childhood asthma. Summary Early-life infections are major determinants of asthma development. The pathway from early-life infections to asthma is the result of complex interactions between the specific type of the virus, genetic, and environmental factors. Novel intervention strategies that target these infectious agents have been investigated in proofof-concepts trials, and further study is necessary to determine their capacity for asthma prevention.

Original languageEnglish
Pages (from-to)172-178
Number of pages7
JournalCurrent Opinion in Allergy and Clinical Immunology
Volume16
Issue number2
DOIs
StatePublished - 2016
Externally publishedYes

Funding

FundersFunder number
National Center for Advancing Translational SciencesUL1TR000448

    Keywords

    • asthma
    • human rhinovirus
    • infections
    • microbiome
    • respiratory syncytial virus

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