By: Tavis Anderson | 10/18/2019 Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
Influenza A viruses (IAV) that circulate in North American pigs maintain a high degree of diversity determined by the hemagglutinin (HA) gene, especially those of the H1 subtype. Genetic diversity is further increased by the bidirectional transmission of IAV between swine and humans and the subsequent processes of antigenic shift and drift. Such evolution can be the basis for changes in antigenic properties of IAV that lead to vaccine failure. Here, we characterized the genetic and antigenic evolution of contemporary swine H1N1 and H1N2 viruses. We compiled a comprehensive dataset of more than 3000 HA genes, and applied Bayesian phylodynamic methods to infer how immune selection, and changes in viral population size, impacted genetic and antigenic diversity. We achieved these analyses using 1-2 dedicated nodes on Ceres, with jobs taking 5-10 days to complete. Our data revealed contrasting patterns of evolution across the known H1 genetic lineages: while the classical swine H1 viruses evolved within established genetic clades, the human-seasonal swine H1 viruses rapidly diversified into three antigenically distinct genetic clades. Further characterization revealed that a few key amino acid mutations were associated with antigenic divergence. The continued genetic and antigenic evolution of contemporary H1 viruses has resulted in vaccines with reduced efficacy, and the observed genetic and antigenic diversity represents a challenge to public health initiatives that attempt to minimize swine-to-human IAV transmission.
Ceres Note: We used 1-2 dedicated nodes on Ceres, run times ranged from 5-10 days (i.e., we used medium/long queues). The advantage here is our prior jobs used CIPRES (max run time of 168 hours/7 days).
Citation: Rajao, D.S., Anderson, T.K., Kitikoon, P., Stratton, J., Lewis, N.S., Vincent, A.L. 2018. Antigenic and genetic evolution of contemporary swine H1 influenza viruses in the United States. Virology, 518:45-54, https://doi.org/10.1016/j.virol.2018.02.006.