Our results demonstrate that the purchase of high level oseltamivir resistance, via the NA R292K mutation, Can appreciably impair the sialidase activity of the H7N9 NA without compromising viral replication, Virulence or transmissibility in these trial and error models. We hypothesize that repair of virus fitness is enabled, especially in part, By contingency, compensatory changes in the expression of HA. the creation of oseltamivir resistance, Unaccompanied by demonstrable losses of replicative potential in vitro or of virulence or transmissibility in vivo, Underscores the multigenic and sometimes capricious nature of fitness in influenza A viruses,

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