Introduction: The segmented nature of influenza A viruses (IAV) allows reassortment when two strains co-infect a cell, which can lead to the emergence of novel pandemic strains. There is little or no pre-existing immunity in the human population, as occurred in the 1957 and 1968 influenza pandemics.
Methods: We have used two complementary approaches to understand the molecular factors that led to the emergence of the 1957 and 1968 pandemic strains by reassortment. A nine-plasmid competitive transfection model to evaluate bias of incorporation of gene segments into progeny virions one at a time, and sequencing of psoralen-crosslinked, ligated, and selected hybrids (SPLASH), which maps RNA interactions between segments by high-throughput sequencing.
Results: We generated plasmids from A/Singapore/57(H2N2) and A/Hong Kong/68(H3N2) pandemic viruses and precursor viruses circulating in 1956 and 1967. Competitive transfection experiments were used to model reassortment that selected the HA, NA and PB1 genes of avian viruses over those of previously circulating human viruses. SPLASH was performed on wild-type (WT) A/Northern Territory/68 virus as well as A/PR/8/34 (PR8) reassortant viruses containing gene segments derived from 1956/1957 or 1967/1968 viruses. We showed that the PB1 gene segments of both pandemic viruses were preferentially selected over those of precursor circulating viruses in the presence of their cognate pandemic NA gene segments, and that selection was driven by two high-frequency interactions between these segments.