PandemieGrippaleV1, PubMed, Checkpoint, bibRecord, 000878

Virulence determinants of pandemic A(H1N1)2009 influenza virus in a mouse model.

Identifieur interne : 000878 ( PubMed/Checkpoint ); précédent : 000877; suivant : 000879

Virulence determinants of pandemic A(H1N1)2009 influenza virus in a mouse model.

Auteurs : Ryuta Uraki [Japon] ; Maki Kiso ; Kyoko Shinya ; Hideo Goto ; Ryo Takano ; Kiyoko Iwatsuki-Horimoto ; Kazuo Takahashi ; Rod S. Daniels ; Olav Hungnes ; Tokiko Watanabe ; Yoshihiro Kawaoka [États-Unis]

Source :

Journal of virology [ 1098-5514 ] ; 2013.

RBID : pubmed:23221570

Descripteurs français

KwdFr :
- Animaux, Facteurs de virulence (génétique), Facteurs de virulence (métabolisme), Femelle, Humains, Infections à Orthomyxoviridae (anatomopathologie), Infections à Orthomyxoviridae (virologie), Modèles animaux de maladie humaine, Protéines virales (génétique), Protéines virales (métabolisme), Souris, Souris de lignée BALB C, Sous-type H1N1 du virus de la grippe A (génétique), Sous-type H1N1 du virus de la grippe A (isolement et purification), Sous-type H1N1 du virus de la grippe A (pathogénicité), Virulence, Virus recombinants (génétique), Virus recombinants (isolement et purification), Virus recombinants (pathogénicité).
MESH :
- anatomopathologie : Infections à Orthomyxoviridae.
- génétique : Facteurs de virulence, Protéines virales, Sous-type H1N1 du virus de la grippe A, Virus recombinants.
- isolement et purification : Sous-type H1N1 du virus de la grippe A, Virus recombinants.
- métabolisme : Facteurs de virulence, Protéines virales.
- pathogénicité : Sous-type H1N1 du virus de la grippe A, Virus recombinants.
- virologie : Infections à Orthomyxoviridae.
- Animaux, Femelle, Humains, Modèles animaux de maladie humaine, Souris, Souris de lignée BALB C, Virulence.

English descriptors

KwdEn :
- Animals, Disease Models, Animal, Female, Humans, Influenza A Virus, H1N1 Subtype (genetics), Influenza A Virus, H1N1 Subtype (isolation & purification), Influenza A Virus, H1N1 Subtype (pathogenicity), Mice, Mice, Inbred BALB C, Orthomyxoviridae Infections (pathology), Orthomyxoviridae Infections (virology), Reassortant Viruses (genetics), Reassortant Viruses (isolation & purification), Reassortant Viruses (pathogenicity), Viral Proteins (genetics), Viral Proteins (metabolism), Virulence, Virulence Factors (genetics), Virulence Factors (metabolism).
MESH :
- chemical , genetics : Viral Proteins, Virulence Factors.
- genetics : Influenza A Virus, H1N1 Subtype, Reassortant Viruses.
- isolation & purification : Influenza A Virus, H1N1 Subtype, Reassortant Viruses.
- chemical , metabolism : Viral Proteins, Virulence Factors.
- pathogenicity : Influenza A Virus, H1N1 Subtype, Reassortant Viruses.
- pathology : Orthomyxoviridae Infections.
- virology : Orthomyxoviridae Infections.
- Animals, Disease Models, Animal, Female, Humans, Mice, Mice, Inbred BALB C, Virulence.

Abstract

A novel swine-origin H1N1 influenza virus [A(H1N1)pdm09 virus] caused the 2009 influenza pandemic. Most patients exhibited mild symptoms similar to seasonal influenza, but some experienced severe clinical signs and, in the worst cases, died. Such differences in symptoms are generally associated with preexisting medical conditions, but recent reports indicate the possible involvement of viral factors in clinical severity. To better understand the mechanism of pathogenicity of the A(H1N1)pdm09 virus, here, we compared five viruses that are genetically similar but were isolated from patients with either severe or mild symptoms. In a mouse model, A/Norway/3487/2009 (Norway3487) virus exhibited greater pathogenicity than did A/Osaka/164/2009 (Osaka164) virus. By exploiting reassortant viruses between these two viruses, we found that viruses possessing the hemagglutinin (HA) gene of Norway3487 in the genetic background of Osaka164 were more pathogenic in mice than other reassortant viruses, indicating a role for HA in the high virulence of Norway3487 virus. Intriguingly, a virus possessing HA, NA, and NS derived from Norway3487 exhibited greater pathogenicity in mice in concert with PB2 and PB1 derived from Osaka164 than did the parental Norway3487 virus. These findings demonstrate that reassortment between A(H1N1)pdm09 viruses can lead to increased pathogenicity and highlight the need for continued surveillance of A(H1N1)pdm09 viruses.

DOI: 10.1128/JVI.01565-12
PubMed: 23221570

Affiliations:

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 000B42
to stream PubMed, to step Curation: 000B42

Links to Exploration step

pubmed:23221570

Le document en format XML

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<front><div type="abstract" xml:lang="en">A novel swine-origin H1N1 influenza virus [A(H1N1)pdm09 virus] caused the 2009 influenza pandemic. Most patients exhibited mild symptoms similar to seasonal influenza, but some experienced severe clinical signs and, in the worst cases, died. Such differences in symptoms are generally associated with preexisting medical conditions, but recent reports indicate the possible involvement of viral factors in clinical severity. To better understand the mechanism of pathogenicity of the A(H1N1)pdm09 virus, here, we compared five viruses that are genetically similar but were isolated from patients with either severe or mild symptoms. In a mouse model, A/Norway/3487/2009 (Norway3487) virus exhibited greater pathogenicity than did A/Osaka/164/2009 (Osaka164) virus. By exploiting reassortant viruses between these two viruses, we found that viruses possessing the hemagglutinin (HA) gene of Norway3487 in the genetic background of Osaka164 were more pathogenic in mice than other reassortant viruses, indicating a role for HA in the high virulence of Norway3487 virus. Intriguingly, a virus possessing HA, NA, and NS derived from Norway3487 exhibited greater pathogenicity in mice in concert with PB2 and PB1 derived from Osaka164 than did the parental Norway3487 virus. These findings demonstrate that reassortment between A(H1N1)pdm09 viruses can lead to increased pathogenicity and highlight the need for continued surveillance of A(H1N1)pdm09 viruses.</div>
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<Abstract><AbstractText>A novel swine-origin H1N1 influenza virus [A(H1N1)pdm09 virus] caused the 2009 influenza pandemic. Most patients exhibited mild symptoms similar to seasonal influenza, but some experienced severe clinical signs and, in the worst cases, died. Such differences in symptoms are generally associated with preexisting medical conditions, but recent reports indicate the possible involvement of viral factors in clinical severity. To better understand the mechanism of pathogenicity of the A(H1N1)pdm09 virus, here, we compared five viruses that are genetically similar but were isolated from patients with either severe or mild symptoms. In a mouse model, A/Norway/3487/2009 (Norway3487) virus exhibited greater pathogenicity than did A/Osaka/164/2009 (Osaka164) virus. By exploiting reassortant viruses between these two viruses, we found that viruses possessing the hemagglutinin (HA) gene of Norway3487 in the genetic background of Osaka164 were more pathogenic in mice than other reassortant viruses, indicating a role for HA in the high virulence of Norway3487 virus. Intriguingly, a virus possessing HA, NA, and NS derived from Norway3487 exhibited greater pathogenicity in mice in concert with PB2 and PB1 derived from Osaka164 than did the parental Norway3487 virus. These findings demonstrate that reassortment between A(H1N1)pdm09 viruses can lead to increased pathogenicity and highlight the need for continued surveillance of A(H1N1)pdm09 viruses.</AbstractText>
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Virulence determinants of pandemic A(H1N1)2009 influenza virus in a mouse model.

Virulence determinants of pandemic A(H1N1)2009 influenza virus in a mouse model.

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