Summary auto-generated
Researchers identified novel H1N2 influenza A viruses in British pigs starting in 1994 and analyzed their genetic origins through antigenic and molecular testing. The haemagglutinin (HA) gene was most closely related to human H1N1 viruses circulating in the early 1980s, while the neuraminidase gene resembled human-derived swine H3N2 viruses. Notably, genes encoding internal proteins (PB2, PB1, PA, NP, M, NS) matched avian viruses recently circulating in European pigs. Phylogenetic analysis showed the H1N2 HA gene branched from the human lineage around 1980, then evolved independently in pigs. The authors propose these viruses arose through multiple reassortment events: first between human H1N1 and swine H3N2 viruses shortly after 1980, then later between the resulting H1N2 virus and avian-like swine H1N1 viruses. This created genetically heterogeneous virus populations cocirculating in pigs, demonstrating that complex reassortment and replication can occur undetected in pigs for years before clinical disease emerges.
Key findings
- Novel H1N2 swine viruses in Great Britain contain a hybrid genome: human-derived HA and NA genes combined with six avian-origin internal protein genes
- Phylogenetic analysis indicates the HA gene transferred from humans to pigs around 1980 and subsequently evolved as a distinct lineage independent of human influenza
- These H1N2 viruses represent a unique genotype not previously reported, distinguished from earlier H1N2 viruses in pigs and humans by their specific combination of human and avian genetic elements
- Multiple genetic reassortment events likely produced these viruses through sequential mixing of human H1N1, swine H3N2, and avian-like swine H1N1 viruses over several years
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Abstract
Novel H1N2 influenza A viruses which were first detected in pigs in Great Britain in 1994 were examined antigenically and genetically to determine their origins and establish the potential mechanisms for genetic reassortment. The haemagglutinin (HA) of all swine H 1 N2 viruses examined was most closely related to, but clearly distinguishable both antigenically and genetically from, the HA of human H1N1 viruses which circulated in the human population during the early 1 980s. Phylogenetic analysis of the HA gene revealed that the swine H 1 N2 viruses formed a distinct branch on the human lineage and were probably introduced to pigs shortly after 1980. Following apparent transfer to pigs the HA gene underwent genetic variation resulting in the establishment and cocirculation of genetically and antigenically heterogeneous virus populations. Genetic analyses of the other RNA segments of all swine H1N2 viruses indicated that the neuraminidase gene was most closely related to those of early 'human-like' swine H3N2 viruses, whilst the RNA segments encoding PB2, PB1, PA, NP, M and NS were related most closely to those of avian viruses, which have been circulating recently in pigs in Northern Europe. The potential mechanisms and probable progenitor strains for genetic reassortment are discussed, but we propose that the swine H1N2 viruses examined originated following multiple genetic reassortment, initially involving human H1N1 and 'human-like' swine H3N2 viruses, followed by reassortment with 'avian-like' swine H1N1 virus. These findings suggest multiple reassortment and replication of influenza viruses may occur in pigs many years before their detection as clinical entities.