Common Respiratory Viruses in Lower Airways of Patients with Acute Hypersensitivity Pneumonitis

Hypersensitivity pneumonitis (HP), a lung disease with "flulike" symptoms, results from repeated exposures to well defined, nonpathogenic antigens. This study examined whether respiratory viruses are present in the lower airways, the likely site of hypersensitivity reaction, in patients wi...

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Bibliographic Details
Published in:American journal of respiratory and critical care medicine Vol. 159; no. 4; pp. 1316 - 1322
Main Authors: DAKHAMA, AZZEDDINE, HEGELE, RICHARD G, LAFLAMME, GENEVIeVE, ISRAeL-ASSAYAG, EVELYNE, CORMIER, YVON
Format: Journal Article
Language:English
Published: New York, NY Am Thoracic Soc 01-04-1999
American Lung Association
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Summary:Hypersensitivity pneumonitis (HP), a lung disease with "flulike" symptoms, results from repeated exposures to well defined, nonpathogenic antigens. This study examined whether respiratory viruses are present in the lower airways, the likely site of hypersensitivity reaction, in patients with HP. The polymerase chain reaction (PCR) method was used to test for 10 common respiratory viruses in bronchoalveolar lavage (BAL) cells obtained from patients with acute HP and from unexposed healthy volunteers. Immunocytochemistry was subsequently used to localize viral proteins within BAL cells. The results of PCR showed that influenza A virus was the most frequently detected virus in the BAL cells of our study patients (six of 13) and control subjects (two of six). Influenza A proteins were detected within alveolar macrophages in nine of 13 patients and in two of six control subjects. The number of total BAL cells, but not lymphocytes, was higher in patients with documented influenza A proteins than in patients with no influenza A proteins (p = 0.017) and correlated with the proportion of influenza-A-positive alveolar macrophages (r = 0.7; p = 0.036). This report documents the presence of viruses in the lower airways of patients with acute HP. The findings may imply a potential role for influenza A in the modulation of HP during antigen exposure.
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ISSN:1073-449X
1535-4970
DOI:10.1164/ajrccm.159.4.9807085