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The purpose of this pilot study was to determine whether complement is activated in the upper respiratory tract during experimental influenza virus infection in human volunteers. Seven subjects were challenged with influenza A/Bethesda/1/85 (H3N2), and four subjects received placebo. C3a and C5a concentrations were measured by radioimmunoassay in nasal lavage fluids before challenge and for 8 days after challenge. A significant increase (p less than 0.05) in C3a and C5a concentrations was demonstrated in lavage fluids from subjects who developed influenza illness as compared with uninfected control subjects and infected subjects who remained asymptomatic. Maximal levels of C3a and C5a were detected during the recovery phase of illness. These results suggest that complement is activated in the airway in response to influenza illness.

Host defenses were evaluated in 70 healthy aged volunteers. Individuals who had diseases or who were taking medication known to affect the inflammatory and immune responses were excluded from the study. Volunteers were followed for 24 months to correlate their state of health with the evaluation of host defenses. Polymorphonuclear leukocyte function and the serum opsonic capacity for Escherichia coli and Staphylococcus aureus were normal. Assays of complement components and activity revealed unexplained elevations in native C3 and properdin, normal concentrations of factor B, normal conversion of C3 by inulin, and normal levels of hemolytic complement. The levels of IgG and IgA did not differ from levels noted in younger controls, but the concentration of IgM was decreased and that of IgE increased. The prevalence of autoantibodies was low. None of the volunteers were anergic, but lymphocyte responses to mitogens were depressed in three-day cultures. The number and percentages of E-rosette-forming cells and cells bearing surface IgD or IgM were normal. No lymphopenia was noted.

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