1. Avian influenza viruses infect primary human bronchial epithelial cells unconstrained by sialic acid α2,3 residues.
- Author
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Oshansky CM, Pickens JA, Bradley KC, Jones LP, Saavedra-Ebner GM, Barber JP, Crabtree JM, Steinhauer DA, Tompkins SM, and Tripp RA
- Subjects
- Adolescent, Animals, Cell Differentiation drug effects, Cell Line, Chemokines metabolism, Cilia drug effects, Cilia metabolism, Cilia pathology, Dogs, Epithelial Cells drug effects, Epithelial Cells pathology, Goblet Cells drug effects, Goblet Cells metabolism, Goblet Cells pathology, Humans, Influenza A virus drug effects, Influenza in Birds pathology, Influenza, Human pathology, Male, Neuraminidase pharmacology, Receptors, Cell Surface metabolism, Virus Replication drug effects, Virus Replication physiology, Virus Shedding drug effects, Virus Shedding physiology, Birds virology, Bronchi pathology, Epithelial Cells virology, Influenza A virus physiology, Influenza in Birds virology, Influenza, Human virology, N-Acetylneuraminic Acid metabolism
- Abstract
Avian influenza viruses (AIV) are an important emerging threat to public health. It is thought that sialic acid (sia) receptors are barriers in cross-species transmission where the binding preferences of AIV and human influenza viruses are sias α2,3 versus α2,6, respectively. In this study, we show that a normal fully differentiated, primary human bronchial epithelial cell model is readily infected by low pathogenic H5N1, H5N2 and H5N3 AIV, which primarily bind to sia α2,3 moieties, and replicate in these cells independent of specific sias on the cell surface. NHBE cells treated with neuraminidase prior to infection are infected by AIV despite removal of sia α2,3 moieties. Following AIV infection, higher levels of IP-10 and RANTES are secreted compared to human influenza virus infection, indicating differential chemokine expression patterns, a feature that may contribute to differences in disease pathogenesis between avian and human influenza virus infections in humans.
- Published
- 2011
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