Abstract
Age-stratified sera collected in 2004, 2008 and 2010 in England were evaluated for antibody to swine influenza A(H3N2) and A(H1N1) viruses from the United States or Europe as a measure of population susceptibility to the emergence of novel viruses. Children under 11 years of age had little or no measurable antibody to recent swine H3N2 viruses despite their high levels of antibody to recent H3N2 seasonal human strains. Adolescents and young adults (born 1968–1999) had higher antibody levels to swine H3N2 viruses. Antibody levels to swine H3N2 influenza show little correlation with exposure to recent seasonal H3N2 (A/Perth/16/2009) strains, but with antibody to older H3N2 strains represented by A/Wuhan/359/1995. Children had the highest seropositivity to influenza A(H1N1)pdm09 virus, and young adults had the lowest antibody levels to A/Perth/16/2009. No age group showed substantial antibody levels to A/Aragon/RR3218/2008, a European swine H1N1 virus belonging to the Eurasian lineage. After vaccination with contemporary trivalent vaccine we observed evidence of boosted reactivity to swine H3N2 viruses in children and adults, while only a limited boosting effect on antibody levels to A/Aragon/RR3218/2008 was observed in both groups. Overall, our results suggest that different vaccination strategies may be necessary according to age if swine viruses emerge as a significant pandemic threat.
Highlights
Pigs are considered a mixing vessel for the reassortment of avian, swine and human influenza viruses
Of 59 residues located at antigenic sites, current human and swine North American H3N2 viruses differ at ca. 16 positions
The highest pairwise identity between current North American swine viruses and human H3N2 viruses included in this analysis is shown with A/Wuhan/359/95 (78–83% identity at antigenic sites, 94% for the entire HA), which is consistent with this virus being an ancestor for the HA segment of recent and classic North American swine influenza A(H3N2) viruses (swH3N2) viruses
Summary
Pigs are considered a mixing vessel for the reassortment of avian, swine and human influenza viruses. By the late 1990s, different subtypes (H1N1, H3N2 and H1N2) had emerged and became predominant among North American pig herds [3]. These swine influenza A viruses acquired avian, human, and swine virus gene segments through reassortment [3,4] and various genetic lineages can be distinguished within each subtype [4]. In Europe, swine influenza is primarily caused by the aforementioned subtypes Their antigenic and genetic characteristics differ significantly from those found in North America and Asia [5,6]. Genetic diversity has been expanded through multiple introductions of influenza viruses from other animal hosts into pig herds, including from humans [7], most recently demonstrated with A(H1N1)pdm virus in Europe, Asia, and the Americas [6,8,9]
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