001) and 65% versus 39% (P < 0.001), respectively.

Among placebo recipients, IgA response rates were generally comparable for subjects with and without a HAI response: 22% versus 30% for A/H1N1 (P = 0.5), 41% versus 28% for A/H3N2 (P = 0.2), and 31% versus 34% for B (P = 0.8). In year 2, 360 placebo recipients and 633 LAIV recipients had data for both HAI and IgA responses. For A/H1N1, A/H3N2 and B, HAI responses were 48% versus 16% (P < 0.001), 42% versus 16% (P < 0.001), and 29% versus 10% (P < 0.001) for LAIV versus placebo recipients, respectively. For LAIV recipients, IgA responses to A/H1N1, A/H3N2, and B were observed among 48% versus 35% (P < 0.001), 51% versus 38% (P < 0.001)

and 48% versus 36% (P < 0.001) of those with and without a HAI response, respectively. As in year 1, IgA responses among placebo recipients ABT-888 ic50 were generally comparable for subjects with and without a HAI response: 21% versus 33% for A/H1N1 (P = 0.1), 26% versus 28% for A/H3N2 (P = 0.9), and 42% versus 27% for B (P = 0.1). selleck inhibitor Based on pooled data from all 3 studies, in years 1 and 2, the mean postvaccination strain-specific to total IgA ratio was 3.1-fold higher (P < 0.01) and 2.0-fold higher (P = 0.03) among LAIV recipients with no culture-confirmed influenza illness compared with LAIV recipients who developed culture-confirmed influenza illness ( Table 3). For each individual study and each type/subtype, mean postvaccination IgA ratios were generally higher among LAIV recipients with no evidence of influenza illness,

although no individual comparison reached statistical significance. When the analysis was restricted to culture-confirmed illness due to vaccine-matched strains, a 3.0-fold difference in IgA ratios between those with and without illness was still present among LAIV recipients in year 1 (P = 0.02). However, in year 2, there were very few subjects who developed vaccine-matched influenza illness (N = 13); Terminal deoxynucleotidyl transferase the IgA ratio was 1.4-fold higher among those without influenza illness but this difference was not statistically significant (P = 0.59). In year 2 of study 3, there was a high incidence of influenza illness due to antigenically mismatched influenza B strains, due to significant circulation of viruses from the influenza B lineage not included in the vaccine; the B/Yamagata lineage strain B/Victoria/504/2000 was included in the vaccine but B/Hong Kong/1351/2002-like viruses of the B/Victoria lineage Modulators circulated. In year 2 of study 3, the mean IgA ratio against the vaccine-matched influenza B antigen was 1.8-fold higher among those subjects without illness compared with those with illness due to opposite lineage B strains (P = 0.15).