H1N1pdm, with positive selection at least during crossspecies transmission. A number of different amino acid mutations that could confer new functionalities to the new virus were reported worldwide, including those related to increased pathogenicity or antiviral resistance ( Table 2) . Polymorphism at position 239 in HA has been associated with severe clinical outcomes, especially in immunocompromised patients; in particular, substitution 239G was found to correlate with fatal outcomes in different countries [17, 18] . Furthermore, this mutation can arise de novo from wildtype (D239) virus in the same patient throughout the disease course [19] . Mutation at position 239 can induce alterations in the receptor binding site, and 239G mutants bind a broader range of 2-3-linked sialyl receptors sequences expressed on cells from the lower respiratory tract, which suggested that its presence could be responsible for the exacerbation of disease [20] . Mutants 239E target mainly non-ciliated cells. We found no significant difference between sequences bearing mutations 239G (2.6%) and 239E (5.5%). The low percentage of global circulation of mutants 239G found in this study is in accordance with its lower potential to transmit to other individuals [21] .