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To the editor: The preferential binding of influenza virus to sialic acid-α2,3-galactose (α2,3 receptor) or sialic acid-α2,6-galactose (α2,6 receptors) may determine its tropism as α2,3 and α2,6 receptors are dominant on lower and upper respiratory cells respectively [1]. The recent glycan microarray analysis suggested that the haemagglutinin (HA) D222G substitution could cause a shift from α2,6 receptors to the mixed α2,3/α2,6 receptors specificity which might increase binding to α2,3 receptors [2] and contribute to severity of disease. This substitution in the HA gene has been reported in samples of viruses obtained from cases with mild to severe illness from around 20 countries, areas and territories [3]. A recent study from Norway has evaluated the clinical relevance of this substitution with severe and mild cases [4]. In an attempt to understand the relevance of HA D222G substitution among pandemic influenza A (H1N1) causing infections in Hong Kong, HA gene sequences from respiratory specimens and virus isolates of severe and non-severe cases were examined. Cases were individuals who had laboratory confirmed pandemic H1N1 influenza virus by either viral culture or reverse transcription PCR (RT-PCR) of respiratory specimens [5]. The severe cases were individuals classified by the attending physician as being in a serious or critical condition.

Association of D222G substitution in haemagglutinin of 2009 pandemic influenza A (H1N1) with severe disease