Literature detail

Avian influenza viruses infect primary human bronchial epithelial cells unconstrained by sialic acid α2,3 residues.

Christine M Oshansky¹ Jennifer A Pickens Konrad C Bradley Les P Jones Geraldine M Saavedra-Ebner James P Barber Jackelyn M Crabtree David A Steinhauer S Mark Tompkins Ralph A Tripp

Affiliations 1 institutions

Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, United States of America.

PMID 21731666 2011 PLoS One eng ppublish

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Article

Publication summary

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.

Adolescent Animals Birds Bronchi Cell Differentiation Cell Line Chemokines Cilia Dogs Epithelial Cells Goblet Cells Humans Influenza A virus Influenza in Birds Influenza, Human Male N-Acetylneuraminic Acid Neuraminidase

Structured evidence records

Evidence records

6 total

Host Range Experiment 3 records

Host Range Experiment Extraction confidence 0.95

Key finding

Low pathogenic avian influenza H5N1, H5N2, and H5N3 viruses infected and replicated in primary human bronchial epithelial cells, indicating these avian viruses can infect human respiratory cells without requiring sialic acid α2,3 residues.

Virus

Host

Location

Supporting text

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.

Method: experimental infection; replication assay
Experimental system: in vitro cell culture

Host Range Experiment Extraction confidence 0.95

Key finding

Low pathogenic avian influenza H5N2 virus infected and replicated in primary human bronchial epithelial cells, indicating infection independent of sialic acid α2,3 residues.

Virus

Host

Location

Supporting text

Method: experimental infection; replication assay
Experimental system: in vitro cell culture

Host Range Experiment Extraction confidence 0.95

Key finding

Low pathogenic avian influenza H5N3 virus infected and replicated in primary human bronchial epithelial cells independently of sialic acid α2,3 residues.

Virus

Host

Location

Supporting text

Method: experimental infection; replication assay
Experimental system: in vitro cell culture

Receptor Usage 3 records

Receptor Usage Extraction confidence 0.98

Key finding

Low pathogenic avian influenza H5N1, H5N2, and H5N3 viruses infect primary human bronchial epithelial cells independently of sialic acid α2,3 receptor residues.

Virus

Host

Location

Supporting text

NHBE cells treated with neuraminidase prior to infection are infected by AIV despite removal of sia α2,3 moieties, showing that low pathogenic H5N1, H5N2, and H5N3 avian influenza viruses replicate independently of sialic acid α2,3 residues on cell surfaces.

Method: neuraminidase treatment; infection assay
Receptors: sialic acid α2,3

Receptor Usage Extraction confidence 0.98

Key finding

Low pathogenic avian influenza H5N2 viruses infect primary human bronchial epithelial cells independently of sialic acid α2,3 receptor residues.

Virus

Host

Location

Supporting text

NHBE cells treated with neuraminidase prior to infection are infected by AIV despite removal of sia α2,3 moieties, showing that low pathogenic H5N2 avian influenza viruses replicate independently of sialic acid α2,3 residues on cell surfaces.

Method: neuraminidase treatment; infection assay
Receptors: sialic acid α2,3

Receptor Usage Extraction confidence 0.98

Key finding

Low pathogenic avian influenza H5N3 viruses infect primary human bronchial epithelial cells independently of sialic acid α2,3 receptor residues.

Virus

Host

Location

Supporting text

NHBE cells treated with neuraminidase prior to infection are infected by AIV despite removal of sia α2,3 moieties, showing that low pathogenic H5N3 avian influenza viruses replicate independently of sialic acid α2,3 residues on cell surfaces.

Method: neuraminidase treatment; infection assay
Receptors: sialic acid α2,3

Citation context

References

64 references

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Evidence overview

Evidence 6

Types 2

Virus 3

Host 3

Evidence types

Host Range Experiment 3 Receptor Usage 3

Linked entities

Viruses

Hosts

Locations

Publication metadata

Journal: PloS one
Volume / Issue / Pages: 6 / 6 / e21183
ISSN: 1932-6203
Journal country: United States
DOI: 10.1371/journal.pone.0021183