GrippeCanadaV3, Main, Exploration, bibRecord, 000436

Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding.

Identifieur interne : 000436 ( Main/Exploration ); précédent : 000435; suivant : 000437

Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding.

Auteurs : Allen C. Bateman [États-Unis] ; Marc G. Busch ; Alexander I. Karasin ; Christopher W. Olsen

Source :

Influenza and other respiratory viruses [ 1750-2659 ] ; 2012.

RBID : pubmed:22353399

Descripteurs français

KwdFr :
- Acide N-acétyl-neuraminique (métabolisme), Animaux, Attachement viral, Cellules cultivées, Cellules épithéliales (virologie), Glycoprotéine hémagglutinine du virus influenza (génétique), Glycoprotéine hémagglutinine du virus influenza (métabolisme), Génétique inverse, Minnesota, Ontario, Protéines mutantes (génétique), Protéines mutantes (métabolisme), Sous-type H3N2 du virus de la grippe A (isolement et purification), Sous-type H3N2 du virus de la grippe A (pathogénicité), Sous-type H3N2 du virus de la grippe A (physiologie), Suidae, Virus recombinants, États-Unis d'Amérique.
MESH :
- génétique : Glycoprotéine hémagglutinine du virus influenza, Protéines mutantes.
- isolement et purification : Sous-type H3N2 du virus de la grippe A.
- métabolisme : Acide N-acétyl-neuraminique, Glycoprotéine hémagglutinine du virus influenza, Protéines mutantes.
- pathogénicité : Sous-type H3N2 du virus de la grippe A.
- physiologie : Sous-type H3N2 du virus de la grippe A.
- virologie : Cellules épithéliales.
- Animaux, Attachement viral, Cellules cultivées, Génétique inverse, Minnesota, Ontario, Suidae, Virus recombinants, États-Unis d'Amérique.
Wicri :
- geographic : États-Unis.

English descriptors

KwdEn :
- Animals, Cells, Cultured, Epithelial Cells (virology), Hemagglutinin Glycoproteins, Influenza Virus (genetics), Hemagglutinin Glycoproteins, Influenza Virus (metabolism), Influenza A Virus, H3N2 Subtype (isolation & purification), Influenza A Virus, H3N2 Subtype (pathogenicity), Influenza A Virus, H3N2 Subtype (physiology), Minnesota, Mutant Proteins (genetics), Mutant Proteins (metabolism), N-Acetylneuraminic Acid (metabolism), Ontario, Reassortant Viruses, Reverse Genetics, Swine, United States, Virus Attachment.
MESH :
- chemical , genetics : Hemagglutinin Glycoproteins, Influenza Virus, Mutant Proteins.
- chemical , metabolism : Hemagglutinin Glycoproteins, Influenza Virus, Mutant Proteins, N-Acetylneuraminic Acid.
- geographic : Minnesota, Ontario, United States.
- isolation & purification : Influenza A Virus, H3N2 Subtype.
- pathogenicity : Influenza A Virus, H3N2 Subtype.
- physiology : Influenza A Virus, H3N2 Subtype.
- virology : Epithelial Cells.
- Animals, Cells, Cultured, Reassortant Viruses, Reverse Genetics, Swine, Virus Attachment.

Abstract

BACKGROUND

In the late 1990s, triple reassortant H3N2 influenza A viruses emerged and spread widely in the US swine population. We have shown previously that an isolate representative of this virus-lineage, A/Swine/Minnesota/593/99 (Sw/MN), exhibits phenotypic differences compared to a wholly human-lineage H3N2 virus isolated during the same time period, A/Swine/Ontario/00130/97 (Sw/ONT). Specifically, Sw/MN was more infectious for pigs and infected a significantly higher proportion of cultured primary swine respiratory epithelial cells (SRECs). In addition, reverse genetics-generated Sw/MN × Sw/ONT reassortant and point mutant viruses demonstrated that the infectivity phenotypes in SRECs were strongly dependent on three amino acids within the hemagglutinin (HA) gene.

OBJECTIVES

To determine the mechanism by which Sw/MN attains higher infectivity than Sw/ONT in SRECs.

METHODS

A/Swine/Minnesota/593/99, Sw/ONT, and mutant (reverse genetics-generated HA reassortant and point mutant) viruses were compared at various HA-mediated stages of infection: initial sialic acid binding, virus entry, and the pH of virus-endosome fusion.

RESULTS/CONCLUSIONS

Sialic acid binding was the sole stage where virus differences directly paralleled infectivity phenotypes in SRECs, indicating that binding is the primary mechanism responsible for differences in the infectivity levels of Sw/MN and Sw/ONT.

DOI: 10.1111/j.1750-2659.2012.00333.x
PubMed: 22353399

Affiliations:

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Le document en format XML

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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>In the late 1990s, triple reassortant H3N2 influenza A viruses emerged and spread widely in the US swine population. We have shown previously that an isolate representative of this virus-lineage, A/Swine/Minnesota/593/99 (Sw/MN), exhibits phenotypic differences compared to a wholly human-lineage H3N2 virus isolated during the same time period, A/Swine/Ontario/00130/97 (Sw/ONT). Specifically, Sw/MN was more infectious for pigs and infected a significantly higher proportion of cultured primary swine respiratory epithelial cells (SRECs). In addition, reverse genetics-generated Sw/MN × Sw/ONT reassortant and point mutant viruses demonstrated that the infectivity phenotypes in SRECs were strongly dependent on three amino acids within the hemagglutinin (HA) gene.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>OBJECTIVES</b>
</p>
<p>To determine the mechanism by which Sw/MN attains higher infectivity than Sw/ONT in SRECs.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>A/Swine/Minnesota/593/99, Sw/ONT, and mutant (reverse genetics-generated HA reassortant and point mutant) viruses were compared at various HA-mediated stages of infection: initial sialic acid binding, virus entry, and the pH of virus-endosome fusion.</p>
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<div type="abstract" xml:lang="en"><p><b>RESULTS/CONCLUSIONS</b>
</p>
<p>Sialic acid binding was the sole stage where virus differences directly paralleled infectivity phenotypes in SRECs, indicating that binding is the primary mechanism responsible for differences in the infectivity levels of Sw/MN and Sw/ONT.</p>
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Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding.

Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding.

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