Viral-induced inflammation in interstitial lung diseases.

Abstract

Viruses have long been implicated as either causative agents or propagators of inflammation in interstitial lung diseases. To date, culture of lung tissue specimens or bronchoalveolar lavage has failed to provide evidence of viable viral organisms. Indirect evidence comes from studies reporting serologic evidence of exposure to numerous viruses in individuals with a variety of interstitial lung diseases. A link between viral infection and interstitial lung diseases also has been suggested by some studies that amplified viral DNA from lung biopsy specimens. The lack of reproducibility of some of these studies suggests that some of these findings may have been false-positive results generated by the extreme sensitivity of the molecular methods used. Furthermore, amplification of viral genomic components from tissue specimens does not necessarily imply that the virus had a direct role in causing the lung injury. There is no definitive evidence that viruses participate in the pathogenesis of idiopathic pulmonary fibrosis, sarcoidosis, and Langerhans' cell histiocytosis. It is possible that some viruses may precipitate hypersensitivity pneumonitis in predisposed individuals, and occasional cases of uncommon interstitial lung diseases have been reported to occur during the course of well-documented viral infections, indicating that, at least in some situations, viruses may be the primary cause of interstitial lung disease. The lack of definitive evidence implicating viral infection as a cause of interstitial lung diseases does not rule out a potential role of viruses as a triggering event that may be important for the development of interstitial lung disease in predisposed individuals.