A complete understanding of the viral kinetics requires investigation of the HA/NA balance. It has been shown that the A/Brisbane/59/2007-like strains of the 2007-2009 influenza seasons differ from earlier H1N1 seasonal strains by a few amino acid substitutions in the HA gene [25] , but none of these involve interaction with the receptor and are therefore not likely to have influenced the changes in fitness. We have recently sequenced the entire genomes of our A/Brisbane/59/2007 strains, and found three amino acid substitutions in the HA gene for the H275Y mutant compared to the WT strain. Two substitutions, G189V and L264F, do not involve interaction with the receptor, but the third, A193T, lies within the receptor-binding site. This latter substitution has been noted in earlier work in relation to oseltamivir-resistant strains of the influenza virus [48] and an investigation of its influence on viral kinetics is a necessary direction for future work.