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Persistent adenoviral infection and chronic airway obstruction in children
1Department of Pediatrics, University Medical Center Ljubljana, Slovenia.
Insights
Persistent adenovirus infections may cause severe childhood asthma. This study found adenoviral capsid protein in 94% of children with severe, steroid-resistant asthma, suggesting a link between persistent viral infection and disease.
Area of Science:
- Pediatric Pulmonology
- Virology
- Immunology
Background:
- Adenovirus is a known cause of severe childhood bronchiolitis.
- Unremitting airway obstruction in children with asthma, despite steroid therapy, suggests underlying persistent infection.
Purpose of the Study:
- To investigate the hypothesis that persistent adenoviral infection contributes to severe childhood asthma unresponsive to standard therapy.
- To determine the prevalence of adenoviral infection in children with difficult-to-treat asthma.
Main Methods:
- Bronchoalveolar lavage (BAL) was performed on 34 children with severe asthma.
- Monoclonal antibody testing of BAL fluid detected adenoviral capsid protein.
- Adenovirus cultures were performed on BAL fluid samples.
- Control group of children without persistent asthma was also studied.
Main Results:
- Adenoviral capsid protein was detected in 31 of 34 (94%) children with severe asthma.
- Repeat testing confirmed persistent adenoviral presence in 75% of cases.
- Adenovirus cultures were positive in all six tested samples, indicating viral replication.
- No evidence of adenovirus was found in control patients.
Conclusions:
- Persistent and/or latent adenoviral infection may play a role in the pathogenesis of severe childhood asthma.
- Findings suggest adenovirus as a potential factor in steroid-unresponsive asthma.
- Further research into adenoviral persistence in pediatric asthma is warranted.
Abstract:
Previous studies from several laboratories have established that adenovirus is a common cause of severe childhood bronchiolitis. The observation that children with an established history of bronchiolitis subsequently developed unremitting airways obstruction even after adequate steroid therapy led us to postulate that this bronchial obstruction might be due to persistence of an adenoviral infection. This hypothesis was tested by performing bronchoalveolar lavage (BAL) on a group of 34 children with a mean age of 5 yr (range, 14 mo to 14 yr) who showed an unfavorable response to standard corticosteroid and bronchodilator therapy. Analysis of cytospin preparations of BAL fluid at the light-microscopic level, using a monoclonal antibody to detect adenoviral antigens, demonstrated that capsid protein was present in 31 of 34 (94%) of the children examined. Limited repeat studies within 1 yr showed 6 of 8 (75%) were positive twice when tested on two occasions, and that three were positive in all occasions when sampled three times. Cultures of the BAL fluid were also positive for adenovirus in six of six cultures performed, indicating that the virus was in some cases replicating. Similar studies of control patients without persistent asthma showed no evidence of adenovirus. We conclude that persistent and/or latent adenoviral infection may contribute to the pathogenesis of childhood asthma in which there is an unfavorable response to steroid and bronchodilatation therapy.