Pathogenicity and immune response of turkey A(H1N2) influenza virus of swine-origin on turkeys and mice.

Abstract

In 2020, a new swine influenza H1_avN2#E genotype emerged in pig farms in France. Shortly after its emergence in swine, this virus was detected in breeding turkey farms, and was responsible of a zoonotic infection. Phylogenetic analyses previously conducted on viral sequences led to the selection of three viruses: the first strain detected in turkeys, resulting from a recent spillover from swine to turkeys (A); a second virus also detected in turkeys and likely adapted to this species (B); and a swine reference strain (C). In the context of species-barrier crossing, the aim of this study was to characterize in vivo these three viruses in an avian model, the breeding turkey, and in a mammalian model, the mouse. Clinical signs, lesions, viral loads, and immune responses were evaluated. In turkeys inoculated experimentally, all three viruses caused similar very mild clinical signs and no viral shedding. In contrast, in mice, virus A caused marked clinical signs associated with mortality, along with a weak inflammatory response. Conversely, virus C caused few clinical signs but showed a more pronounced inflammatory response. Surprisingly, only two nonsynonymous mutations were present between viruses C and A: K189R in PB1 and E233K in HA. Virus B displayed an intermediate profile. There was no difference in genomic load in the lungs among the three viruses, suggesting that the observed differences in pathogenicity were due to the immune response rather than viral replication.