AIRWAY HYPER-REACTIVITY AND PERIPHERAL AIRWAY DYSFUNCTION IN INFLUENZA A INFECTION

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Abstract
College students (39) with documented nonpneumonitic influenza A/Victoria/3/75/H3N2 infection were studied to examine alterations in pulmonary mechanics and airway reactivity to cholinergic challenge, and to assess the effect of the antiviral agent amantadine on these changes. Thirty-six of the 39 subjects (92%) demonstrated diminished forced flow rates and decreased density-dependent forced flow rates while breathing a H-O2 mixture as compared to an air mixture. On initial evaluation, there was no significant difference in forced flow rates or density dependence between a group of 18 subjects treated with amantadine and 21 subjects given a placebo. The placebo group demonstrated further decreases in density dependence 7 days after initial presentation, but the amantadine group demonstrated a significant increase in density dependence (P < 0.05), which suggested an accelerated improvement in peripheral airway dysfunction in the treated group. After inhalation of carbachol aerosol, 25 subjects showed a significant (P < 0.05) increase in total respiratory resistance that was prolonged and independent of hay fever history. Airway hyperreactivity gradually diminished during a 7 wk period in both groups. There was no significant difference in the initial degree of hyperreactivity or in the rate of improvement between groups. Nonpneumonitic influenza infection may be associated with both an inflammatory response predominantly in the peripheral airways and transient bronchial hyperreactivity. By its antiviral effect, amantadine may arrest the proliferation of virus and associated inflammatory response in peripheral airways, but airway hyperreactivity presumably related to initially damaged airway epithelium is not attenuated by inhibition of viral replication after infection was established.