Avian Influenza Viruses Infect Primary Human Bronchial Epithelial Cells Unconstrained by Sialic Acid alpha 2,3 Residues

• Authors: Christine M. Oshansky, University of Georgia; Jennifer A. Pickens, University of Georgia; Konrad C. Bradley, Emory University; Les P. Jones, University of Georgia; Geraldine M. Saavedra-Ebner, University of Georgia; James P. Barber, University of Georgia; Jackelyn M. Crabtree, University of Georgia; David Steinhauer, Emory University; S. Mark Tompkins, University of Georgia; Ralph A. Tripp, University of Georgia
• Journal Title: PLoS ONE
• Volume: Volume 6, Number 6
• Publisher: Public Library of Science | 2011-06-23, Pages e21183-e21183
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.1371/journal.pone.0021183
• Subjects: Biology, Microbiology; Biology, Virology; Health Sciences, Public Health
• Keywords: Multidisciplinary Sciences; RECEPTOR-BINDING SPECIFICITY; HUMAN AIRWAY EPITHELIUM; I INTERFERON RESPONSE; MAACKIA-AMURENSIS; CYTOKINE RESPONSES; GENE-EXPRESSION; HUMAN ALVEOLAR; HOST-RANGE; H1N1; H5N1; Influenza viruses; Influenza; Sialic acids; Respiratory infections; Viral replication; Influenza A virus; Viral pathogens

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.