Influenza A (H1N1) 2009 pandemic virus: learning from the first wave, preparing for the second

In a short period of two months, the novel influenza A/H1N1 virus has circumnavigated the entire planet leaving behind in its wake approximately 3000 reported deaths worldwide. Fortunately, in many areas around the world, September 2009 brought a lull in the number of new H1N1 infections. This brought welcomed relief in many countries that had earlier experienced high respiratory disease activity in their communities. However, based on previous influenza pandemics, this reprieve may well be short-lived. As the Northern hemisphere approaches its winter months, many experts are now predicting a second wave of influenza A/H1N1 infections. This prediction maybe well placed as all 3 influenza pandemics in the last century reported second or even subsequent waves of new infections, all of which appeared to be more severe than the primary event (ref). The timing of these second waves have varied from 6 months to 3 years and invariably seemed to be linked to the winter months. It is unclear precisely what changes caused the increased severity seen during the second waves; one possibility is the progressive adaptation of the novel influenza virus to its new human host . Molecular analysis, for example, suggests that the 1918 Spanish influenza virus that emerged during the second wave had undergone changes in the hemagglutinin binding site that increased the binding specificity for human receptors. This is thought to have increased the replicative capacity and hence, the pathogenicity of the virus. It is also evident that as the H1N1 2009 pandemic virus continues to spread, opportunities for adaptation that increases virulence will also increase. Nonetheless, the changes needed for such adaptation and for increased virulence are unpredictable and by no means inevitable