Data associated with the publication: The impact of human H3N2 influenza virus reassortment during 2017-18 on increased influenza cases and disease severity: enhanced virus replication and neuraminidase antibody immune evasion

During the 2017-18 influenza season in the United States, there was a high incidence of influenza illness and mortality. However, no apparent mutations were identified in the HA gene segment of dominant H3N2 viruses, and the severity of the season could not be solely attributed to a vaccine mismatch. Clinical samples from the Johns Hopkins Center of Excellence for Influenza Research and Surveillance network during the 2016-17 and 2017-18 influenza seasons were sequenced to target influenza A virus. Phylogenetic trees were constructed based on viral whole genome sequences. Representative viral isolates of the two seasons were characterized in immortalized cell lines and human nasal epithelial cell cultures, and demographic data and clinical outcomes of patients were analyzed. Unique H3N2 reassortment events were observed, resulting in two predominant strains in the 2017-18 season: HA clade 3C.2a2 and clade 3C.3a, which had novel gene segment constellations containing gene segments from HA clade 3C.2a1 viruses. The reassortant re3C.2a2 viruses replicated with faster kinetics and to a higher peak titer compared to the parental 3C.2a2 and 3C.2a1 viruses, which may have contributed to the increased severity. The reassortant re3C.3a was able to infect an older population more effectively compared to the parental 3C.3a, perhaps through evasion of preexisting NA antibodies. Our findings suggest that the increased severity of the 2017-18 influenza season was due in part to two intrasubtypes, co-circulating H3N2 reassortant viruses with fitness advantages over the parental viruses. This information may help inform future vaccine development and public health policies. (2023-08)