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Abstract
Despite a regional decline in influenza A(H1N1)pdm09 virus infections during 2013–14, cases at a Florida hospital were more severe than those during 2009–10. Examined strains had a hemagglutinin polymorphism associated with enhanced binding to lower respiratory tract receptors. Genetic changes in this virus must be monitored to predict the effect of future pandemic viruses.
Highlights
Despite a regional decline in influenza A(H1N1)pdm09 virus infections during 2013–14, cases at a Florida hospital were more severe than those during 2009–10
Of 1,024 patients admitted to the medical intensive care unit (MICU) in 2013–14, a total of 49 had influenza, yielding an admission rate of 4.8%
Cytopathic effects were first apparent and were extensive in MDCK-SIAT2,6-UF cells, followed by MDCK-SIAT2,3-UF, wild-type MDCK cells. These results suggest that the H1N1 virus isolates in our study use both α2-6- and α2-3-sialylglycan receptors, Table
Summary
Providing a potential mechanism by which lower respiratory tract disease can occur. The molecular basis for the ability of the H1N1 viruses to cause severe lower respiratory tract disease was first noted with the 1918 pandemic H1N1 virus [10]. A single amino acid change of aspartic acid at position 225 to glycine (D225G) enabled binding to α2-3- and α2-6-sialylglycans [10,11] The association of this polymorphism with severe and lower respiratory tract disease was noted with the A(H1N1)pdm virus from small subsets of patients during the 2009–10 influenza season [12,13,14]. To determine if this polymorphism existed in the H1N1 viruses isolated in our study, we sequenced viral RNA corresponding to the coding regions of all 8 influenza virus genomic segments from viruses isolated from or detected in 7 patient samples (GenBank sequences KJ645758–KJ645765 and KJ645774–KJ645791) [8]. Changes in health-seeking behavior in 2009–10 versus 2013–14 were not addressed
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