Asthma is characterized by abnormal immune cell accumulation and activation in the airways and consequent dysfunction of specialized parenchymal cells. To date, research strategies aimed at defining asthma pathogenesis have focused on the hypothesis that this altered state is a consequence of an excessive allergen-driven response. However, this view might not fully account for the development of asthma and thus might not lead to curative therapeutics. In this context, it is relevant to consider that asthma might share with paramyxoviral infection a propensity to activate a network of epithelial immune response genes that are part of the innate immune response. More recent results extend this concept by establishing the capacity of a single transient paramyxoviral infection to permanently change airway epithelial behavior and reactivity in a pattern that is remarkably similar to one in asthma and that overlaps with other hypersecretory diseases. The teleology of this chronic response is uncertain, but it might represent an evolving but maladaptive attempt to improve antiviral host defense. Further studies are now required to precisely identify the cellular and molecular events responsible for chronic airway remodeling and hyperreactivity in response to paramyxoviral infection. Definition of the cellular and molecular pathways for viral reprogramming of airway behavior in isolated cell and mouse models will eventually translate into an understanding of how these pathways work in adult and pediatric populations with chronic airway disease, in which the link between viral infection and disease appears strong. Indeed, initial results indicate that viral infection in a specific genetic background might lead to chronic dysfunction of host cell behavior that overlaps with but does not depend on allergy, thereby providing a road on which to drive new disease-modifying strategies.

Original languageEnglish
Pages (from-to)244-247
Number of pages4
JournalJournal of Allergy and Clinical Immunology
Issue number2
StatePublished - Feb 1 2003


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