The impact of respiratory viral infections in patients with cystic fibrosis.

Respiratory viruses have been implicated in pulmonary exacerbations of CF and in the long-term course of pulmonary dysfunction in these patients. However, the data are by no means complete and there is the clear need for more intensive evaluations of the role of viral pathogens in this population. Further controlled prospective studies assessing the impact of viral infections in large cohorts of patients with CF are still necessary. Placebo-controlled, antiviral treatment protocols also should be initiated. In clinical practice at the present time, patients with CF should be assessed for respiratory viral infections, at least at the time of hospitalizations for pulmonary deterioration. This assessment should include obtaining specimens from the respiratory tract for viral cultures and rapid respiratory viral antigen detection. Identifying a respiratory viral infection may alter clinical care. The patient can be isolated appropriately, and it may be possible to reduce the intensive use of expensive and potentially toxic parenteral antibiotics. The role of antiviral therapy in these patients must await further evaluations. The mechanisms of the short- and long-term effects of respiratory viruses in patients with CF have not been defined. However, pathophysiologic studies conducted in normal children and adults allow the development of several plausible hypotheses. The definition of mechanisms of injury in this population must be a priority, since it may influence clinical practice. If airway obstruction is the principal mechanism of viral-induced injury, therapeutic approaches designed to relieve the obstruction would be most appropriate. For example, if the obstruction resulted from induced or aggravated reactive airway disease, the current common practice of prescribing chronic bronchodilator therapy would be appropriate. This therapy might be especially suited to those experiencing frequent viral infections. In addition, the administration of bronchodilators to patients during acute exacerbations of pulmonary disease caused by viruses might be of clinical benefit. If, on the other hand, the principal mechanism of viral-induced injury is found to be through synergistic interaction with bacteria, the current practice of aggressive antimicrobial therapy would remain appropriate.