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Background Influenza A(H1N1)pdm09 virus has been circulating in human population for three epidemic seasons. During this time, monovalent pandemic and trivalent seasonal influenza vaccination against this virus have been offered to Finnish healthcare professionals. It is, however, unclear how well vaccine-induced antibodies recognize different strains of influenza A(H1N1)pdm09 circulating in the population and whether the booster vaccination with seasonal influenza vaccine would broaden the antibody cross-reactivity. Objectives Influenza vaccine-induced humoral immunity against several isolates of influenza A(H1N1)pdm09 virus was analyzed in healthcare professionals. Age-dependent responses were also analyzed. Methods Influenza viruses were selected to represent viruses that circulated in Finland during two consecutive influenza epidemic seasons 2009–2010 and 2010–2011. Serum samples from vaccinated volunteers, age 20–64 years, were collected before and after vaccination with AS03-adjuvanted pandemic and non-adjuvanted trivalent seasonal influenza vaccine that was given 1 year later. Results Single dose of pandemic vaccine induced a good albeit variable antibody response. On day 21 after vaccination, depending on the virus strain, 14–75% of vaccinated had reached antibody titers (≥1:40) considered seroprotective. The booster vaccination 1 year later with a seasonal vaccine elevated the seroprotection rate to 57–98%. After primary immunization, younger individuals (20–48 years) had significantly higher antibody titers against all tested viruses than older persons (49–64 years) but this difference disappeared after the seasonal booster vaccination. Conclusions Even a few amino acid changes in influenza A HA may compromise the vaccine-induced antibody recognition. Older adults (49 years and older) may benefit more from repeated influenza vaccinations.

A total of 102,600 upper respiratory infections (URI) were recorded among young military conscripts in the Finnish Defence Forces during the study period from October 1991 to March 1994. This period covered three outbreaks caused by H3N2-subtype influenza A virus and one outbreak of influenza B. During the 1991/92 outbreak caused by A/Beijing/353/89-like virus, the calculated influenza A incidence was 2,206/10,000 men. During the 1992/93 outbreak when influenza B was the predominant virus, a new drift variant of influenza A that belonged to the lineage of A/Beijing/32/92-like and A/Shangdong/9/93-like viruses circulated but the incidence of influenza A was not more than 1,044/10,000. A higher incidence, 2,810/10,000, was recorded during the 1993/94 outbreak, when the circulating virus was similar to the 1992/93 virus antigenically and with regard to haemagglutinin and neuraminidase (NA) gene sequences. Crossreactive haemagglutination-inhibition antibodies induced in 1991/92 probably were sufficient to restrict the epidemic activity in 1992/93 but no longer in 1993/94. Furthermore, during the 1991/92 outbreak, some of the A/Beijing/353/89-like viruses already had shared the NA sequence markers characteristic of the viruses in 1992/93 and 1993/94, which may also have strengthened protection in 1992/93.

Intraepidemic antigenic and genetic variation was indicated when H3N2-subtype influenza A virus strains isolated during the 1996–1997 epidemic season in Finland were studied for reactivity in the haemagglutination inhibition (HI) assay and for nucleotide sequences coding for the variable HA1 domain of viral haemagglutinin. Thirty prevaccination- and postvaccination-paired sera taken from subjects who had been vaccinated against influenza during the previous autumn were studied for the presence of HI antibody to the homologous vaccine virus A/Nanchang/933/95, and five field strains representing the genetic and antigenic variability of the 1996–1997 epidemic season. The lowest vaccination-induced HI titres in each of the three age groups were detected in the two field strains that had been isolated from vaccinated patients and belonged to two different genetic sublineages. The intraepidemic variability of the 1996–1997 field strains in HI reactivity may be indicative of circulation of virus strains that may be capable of breaking through vaccination-induced immunity better than the other strains. J. Med. Virol. 65:584–589, 2001. © 2001 Wiley-Liss, Inc.