Small airways dysfunction in influenza A virus infection: therapeutic role and potential mode of action of amantadine.

Previous studies have demonstrated alterations in gas exchange and pulmonary mechanics in presumed and documented viral upper respiratory infections. In our laboratory, using sensitive and noninvasive testing, we have demonstrated significant and prolonged alterations of pulmonary mechanics in uncomplicated natural influenza A infection, which implicate increased resistance in small airways as the cause of dysfunction. Amantadine administration in established influenza A infection has been associated with an accelerated improvement of clinical illness and pulmonary physiologic dysfunction. Preliminary study suggests that this is due to neither cholinergic blockade nor bronchodilation.