The H275Y mutation in the neuraminidase (NA) gene (H274Y in N2 numbering), first described in 2000 [10] , is the most frequent mutation associated with oseltamivir-resistance in the N1 subtype, but it had long been thought to critically reduce viral fitness [11] . With a location on the framework residue of the enzyme catalytic site [12] , the mutation has been shown to cause a reduced affinity for the substrate in enzyme activity assays [12, 13] , an impaired viral fitness in vitro [14] [15] [16] , and up to a 100-fold reduction in transmission efficiency in ferrets [14, 17] . For these reasons, strains carrying the H275Y mutation were not thought to be a great concern for public health [10, 18] . During the 2007-2008 influenza season, however, the A/ Brisbane/59/2007-like (H1N1) H275Y mutant emerged and rapidly disseminated worldwide in the apparent absence of antiviral pressure [8, [19] [20] [21] . Recently, our group performed a study on the replicative capacities of the A/Brisbane/59/2007 H275Y mutant strain where we showed that its fitness, based on in vitro and animal studies, was similar to that of its wild-type (WT), oseltamivir-susceptible, counterpart [22] . These observations, and those of others [23] , correlate with the clinical situation encountered in the 2008-2009 season where almost 100% of the A/H1N1 viruses isolated in North America and Europe were resistant to oseltamivir due to the H275Y mutation [1, 19, 23] .