H3N2 genetic variants linked to increased disease severity

Check out the latest (and likely last) work from my time at Johns Hopkins. Phylogenetics were used to identify clade and genotype information for H3N2 viruses circulating during the 2014-2015 influenza season. Interestingly, two mutations were co-selected and become the dominant strain in subsequent seasons. These mutations were an additional glycosylation in the NA protein and a missense mutation in the PB1-F2 causing a proline to appear at position 75 instead of histidine. These co-selected mutations didn't affect virus replication on MDCK cells or MDCK cells overexpressing α2-6 linked sialic acid (the receptor for most human influenza viruses), but did have reduced replication in primary human airway epithelial cells. Despite this, the virus was actually associated with increased coughing and shortness of breath in infected patients. We still have a lot to learn about what makes different infectious agents cause more- or less-severe disease, but studies like this one help on that path.

https://academic.oup.com/ve/article/7/1/veab047/6272594