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Infection of human airway epithelia with H1N1, H2N2, and H3N2 influenza A virus strains.

Identifieur interne : 001802 ( Main/Exploration ); précédent : 001801; suivant : 001803

Infection of human airway epithelia with H1N1, H2N2, and H3N2 influenza A virus strains.

Auteurs : V A Slepushkin [États-Unis] ; P D Staber ; G. Wang ; P B Mccray ; B L Davidson

Source :

RBID : pubmed:11273782

Descripteurs français

English descriptors

Abstract

Three subtypes of influenza A virus cause human disease: H1N1, H2N2, and H3N2. Although all result in respiratory illness, little is known about how these subtypes infect differentiated airway epithelia. Therefore, we assayed A/PR/8/34 (H1N1), A/Japan/305/57 (H2N2), and X31 (H3N2) influenza virus strains for binding and infection on fully differentiated primary cultures of airway epithelia isolated from human bronchus, grown on semiporous filters at an air-liquid interface. In this model system, viral infectivity was highest when virus was applied to the apical versus the basolateral surface; Japan was most infectious, followed by PR8. The X31 strain showed very low levels of infectivity. Confocal microscopy and fluorescence-resonance energy transfer studies indicated that Japan virus could enter and fuse with cellular membranes, while infection with X31 virions was greatly inhibited. Japan virus could also productively infect human trachea explant tissues. These data show that influenza viruses with SAalpha2,3Gal binding specificity, like Japan, productively infect differentiated human airway epithelia from the apical surface. These data are important to consider in the development of pseudotyped recombinant viral vectors for gene transfer to human airway epithelia for gene therapy.

DOI: 10.1006/mthe.2001.0277
PubMed: 11273782


Affiliations:


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Le document en format XML

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<nlm:affiliation>Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA.</nlm:affiliation>
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<term>Antibodies, Viral (biosynthesis)</term>
<term>Bronchi (virology)</term>
<term>Cells, Cultured</term>
<term>Endocytosis</term>
<term>Epithelial Cells (ultrastructure)</term>
<term>Epithelial Cells (virology)</term>
<term>Hemagglutination, Viral (immunology)</term>
<term>Humans</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza A Virus, H2N2 Subtype</term>
<term>Influenza A Virus, H3N2 Subtype</term>
<term>Influenza A virus (immunology)</term>
<term>Influenza A virus (physiology)</term>
<term>Membrane Fusion</term>
<term>Models, Biological</term>
<term>Trachea (virology)</term>
<term>Viral Proteins (biosynthesis)</term>
<term>Virus Replication</term>
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<term>Anticorps antiviraux (biosynthèse)</term>
<term>Bronches (virologie)</term>
<term>Cellules cultivées</term>
<term>Cellules épithéliales (ultrastructure)</term>
<term>Cellules épithéliales (virologie)</term>
<term>Endocytose</term>
<term>Fusion membranaire</term>
<term>Humains</term>
<term>Hémagglutination virale (immunologie)</term>
<term>Modèles biologiques</term>
<term>Protéines virales (biosynthèse)</term>
<term>Réplication virale</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
<term>Sous-type H2N2 du virus de la grippe A</term>
<term>Sous-type H3N2 du virus de la grippe A</term>
<term>Trachée (virologie)</term>
<term>Virus de la grippe A (immunologie)</term>
<term>Virus de la grippe A (physiologie)</term>
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<term>Protéines virales</term>
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<term>Virus de la grippe A</term>
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<term>Influenza A virus</term>
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<term>Epithelial Cells</term>
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<term>Bronches</term>
<term>Cellules épithéliales</term>
<term>Trachée</term>
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<term>Epithelial Cells</term>
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<term>Influenza A Virus, H2N2 Subtype</term>
<term>Influenza A Virus, H3N2 Subtype</term>
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<term>Models, Biological</term>
<term>Virus Replication</term>
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<term>Réplication virale</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
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<div type="abstract" xml:lang="en">Three subtypes of influenza A virus cause human disease: H1N1, H2N2, and H3N2. Although all result in respiratory illness, little is known about how these subtypes infect differentiated airway epithelia. Therefore, we assayed A/PR/8/34 (H1N1), A/Japan/305/57 (H2N2), and X31 (H3N2) influenza virus strains for binding and infection on fully differentiated primary cultures of airway epithelia isolated from human bronchus, grown on semiporous filters at an air-liquid interface. In this model system, viral infectivity was highest when virus was applied to the apical versus the basolateral surface; Japan was most infectious, followed by PR8. The X31 strain showed very low levels of infectivity. Confocal microscopy and fluorescence-resonance energy transfer studies indicated that Japan virus could enter and fuse with cellular membranes, while infection with X31 virions was greatly inhibited. Japan virus could also productively infect human trachea explant tissues. These data show that influenza viruses with SAalpha2,3Gal binding specificity, like Japan, productively infect differentiated human airway epithelia from the apical surface. These data are important to consider in the development of pseudotyped recombinant viral vectors for gene transfer to human airway epithelia for gene therapy.</div>
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