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.

The persistent presence of viruses in the upper respiratory tract of asthmatic children shows a possible connection between viral infections and asthma.

The polymerase chain reaction (PCR) is a powerful method that allows enzymatic amplification of race target nucleic acid sequences. It has been applied to the amplification of viral genomes from paraffin-embedded pathology specimens. However, interpretation of negative results requkes amplification of a housekeeping gene such as b-actin. In the present study we used specific oligonucleotide primers previously designed to amplify both the genomic DNA and the mRNA transcript from paraffin-embedded tissue. These products have predicted sizes of 250 BP and 154 BP, respectively, but our results showed that PCR amplifcation only (without reverse transcription) unexpectedly generated the 1544'

In fatal asthma, lower airway secretions do not show a specific pattern of viral nucleic acid. Intriguingly, these results suggest that the lower respiratory tract may act as a potential reservoir for common respiratory viruses.

No abstract