Participants who

selleck products were 5 years of age or older at the time of sampling were asked to provide blood at recruitment and after each peak in confirmed case detection for paired serology. Age- and sex-standardized estimates of the risk of influenza infection and illness per season in persons 5 years of age or older were reported previously.21 Three influenza seasons were identified in this study period (Table 1). The number of people that provided blood samples spanning each season, the numbers infected as determined by serology and RT-PCR, and their age distribution is shown as supplementary information (Fig. S1). Males, and participants aged less than 5 or in their late teens were under-represented in the group that could be analyzed (Fig. S1). Genetic and antigenic characterization of the viruses isolated and used for serology is shown in supplementary information (Fig. S2 and Table S1). The H1N1 viruses isolated in season one (S1) in 2008 were A/Brisbane/59/2007-like, and B

virus isolates were of the B-Yamagata-lineage and were B/Florida/4/2006-like, representing strains that were antigenically distinct from the pre-study season. The H3N2 viruses isolated in S1 were antigenically A/Brisbane/10/2007-like, as in the pre-study season, and caused few infections. The H3N2 viruses isolated in the second season (S2) in Spring 2009 were antigenically distinct A/Perth/16/2009-like strains, and caused the highest incidence of infection, whereas two

H1N1 isolates were similar to the S1 isolate. HI titers with WHO reference sera against seasonal H1N1 XL184 molecular weight were 1280 against the 2008 H1N1 isolate and 640 against both 2009 H1N1 isolates. The only B virus isolated in 2009 belonged to the B-Victoria lineage, L-gulonolactone oxidase and the National Influenza surveillance system identified a shift in B-lineage predominance from Yamagata to Victoria in 2009. However serology was only performed with a Yamagata lineage virus. The third season (S3) in Autumn 2009, was caused by the pandemic H1N1 2009 strain (A/California/04/2009), which resulted in a high incidence of infection compared to individual seasonal strains. It was not feasible to collect swabs from all cohort participants weekly; hence infections were also identified by HI antibody seroconversion. As in our previous report, seroconversion was defined as at least a 4-fold rise in titer with a post-season titer of at least 40.21 We have recently reported that the pattern of 2-fold increases in HI titer cannot be fully explained by assay variability, and that a reliance on four-fold titer increases to define infection may under estimate the true incidence of infection.24 However, since it is not possible to adjust for assay variability in an individual level analysis we did not apply a 2-fold definition.