In contrast to seasonal influenza in human cases, H1N1pdm infections showed a tropism for the lung similar to H5N1 [6] . The ability of H1N1pdm viruses to infect the lower respiratory track has been attributed to a broader specificity in the binding of the viral hemagglutinin (HA) to a2-3in addition to a2-6-linked sialic acid (SA) receptors [7, 8] . It is reasonable that the lung tropism of the H1N1pdm contributed to the severity of disease in those individuals with preexisting complications such as asthma and chronic obstructive pulmonary disease (COPD) [6, [9] [10] [11] [12] . Data from limited human autopsies and animal studies of various pandemic strains also suggest contribution of the host innate immune response and the virus in the progression of disease [13] [14] [15] [16] .