Aberrant innate immune response in lethal infection of macaques with the 1918 influenza virus.
Identifieur interne : 000455 ( Ncbi/Curation ); précédent : 000454; suivant : 000456Aberrant innate immune response in lethal infection of macaques with the 1918 influenza virus.
Auteurs : Darwyn Kobasa [Canada] ; Steven M. Jones ; Kyoko Shinya ; John C. Kash ; John Copps ; Hideki Ebihara ; Yasuko Hatta ; Jin Hyun Kim ; Peter Halfmann ; Masato Hatta ; Friederike Feldmann ; Judie B. Alimonti ; Lisa Fernando ; Yan Li ; Michael G. Katze ; Heinz Feldmann ; Yoshihiro Kawaoka [États-Unis]Source :
- Nature [ 1476-4687 ] ; 2007.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes, Animaux, Chimiokines (sang), Cytokines (sang), Facteurs temps, Femelle, Grippe humaine (immunologie), Grippe humaine (sang), Grippe humaine (virologie), Humains, Immunité innée (immunologie), Macaca fascicularis (immunologie), Macaca fascicularis (virologie), Modèles animaux de maladie humaine, Poumon (anatomopathologie), Poumon (métabolisme), Poumon (virologie), Régulation de l'expression des gènes, Réplication virale, 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 (immunologie), Sous-type H1N1 du virus de la grippe A (pathogénicité), Séquençage par oligonucléotides en batterie, Taux de survie.
- MESH :
- anatomopathologie : Poumon.
- génétique : Sous-type H1N1 du virus de la grippe A.
- immunologie : Grippe humaine, Immunité innée, Macaca fascicularis, Sous-type H1N1 du virus de la grippe A.
- métabolisme : Poumon.
- pathogénicité : Sous-type H1N1 du virus de la grippe A.
- sang : Chimiokines, Cytokines, Grippe humaine.
- virologie : Grippe humaine, Macaca fascicularis, Poumon.
- Analyse de profil d'expression de gènes, Animaux, Facteurs temps, Femelle, Humains, Modèles animaux de maladie humaine, Régulation de l'expression des gènes, Réplication virale, Souris, Souris de lignée BALB C, Séquençage par oligonucléotides en batterie, Taux de survie.
English descriptors
- KwdEn :
- Animals, Chemokines (blood), Cytokines (blood), Disease Models, Animal, Female, Gene Expression Profiling, Gene Expression Regulation, Humans, Immunity, Innate (immunology), Influenza A Virus, H1N1 Subtype (genetics), Influenza A Virus, H1N1 Subtype (immunology), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza, Human (blood), Influenza, Human (immunology), Influenza, Human (virology), Lung (metabolism), Lung (pathology), Lung (virology), Macaca fascicularis (immunology), Macaca fascicularis (virology), Mice, Mice, Inbred BALB C, Oligonucleotide Array Sequence Analysis, Survival Rate, Time Factors, Virus Replication.
- MESH :
- chemical , blood : Chemokines, Cytokines.
- blood : Influenza, Human.
- genetics : Influenza A Virus, H1N1 Subtype.
- immunology : Immunity, Innate, Influenza A Virus, H1N1 Subtype, Influenza, Human, Macaca fascicularis.
- metabolism : Lung.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- pathology : Lung.
- virology : Influenza, Human, Lung, Macaca fascicularis.
- Animals, Disease Models, Animal, Female, Gene Expression Profiling, Gene Expression Regulation, Humans, Mice, Mice, Inbred BALB C, Oligonucleotide Array Sequence Analysis, Survival Rate, Time Factors, Virus Replication.
Abstract
The 1918 influenza pandemic was unusually severe, resulting in about 50 million deaths worldwide. The 1918 virus is also highly pathogenic in mice, and studies have identified a multigenic origin of this virulent phenotype in mice. However, these initial characterizations of the 1918 virus did not address the question of its pathogenic potential in primates. Here we demonstrate that the 1918 virus caused a highly pathogenic respiratory infection in a cynomolgus macaque model that culminated in acute respiratory distress and a fatal outcome. Furthermore, infected animals mounted an immune response, characterized by dysregulation of the antiviral response, that was insufficient for protection, indicating that atypical host innate immune responses may contribute to lethality. The ability of influenza viruses to modulate host immune responses, such as that demonstrated for the avian H5N1 influenza viruses, may be a feature shared by the virulent influenza viruses.
DOI: 10.1038/nature05495
PubMed: 17230189
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pubmed:17230189Le document en format XML
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<affiliation wicri:level="1"><nlm:affiliation>Respiratory Viruses, Public Health Agency of Canada, Winnipeg, Manitoba R3E 3R2, Canada.</nlm:affiliation>
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<term>Chemokines (blood)</term>
<term>Cytokines (blood)</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>Immunity, Innate (immunology)</term>
<term>Influenza A Virus, H1N1 Subtype (genetics)</term>
<term>Influenza A Virus, H1N1 Subtype (immunology)</term>
<term>Influenza A Virus, H1N1 Subtype (pathogenicity)</term>
<term>Influenza, Human (blood)</term>
<term>Influenza, Human (immunology)</term>
<term>Influenza, Human (virology)</term>
<term>Lung (metabolism)</term>
<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>Macaca fascicularis (immunology)</term>
<term>Macaca fascicularis (virology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Survival Rate</term>
<term>Time Factors</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Animaux</term>
<term>Chimiokines (sang)</term>
<term>Cytokines (sang)</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Grippe humaine (immunologie)</term>
<term>Grippe humaine (sang)</term>
<term>Grippe humaine (virologie)</term>
<term>Humains</term>
<term>Immunité innée (immunologie)</term>
<term>Macaca fascicularis (immunologie)</term>
<term>Macaca fascicularis (virologie)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (métabolisme)</term>
<term>Poumon (virologie)</term>
<term>Régulation de l'expression des gènes</term>
<term>Réplication virale</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Sous-type H1N1 du virus de la grippe A (génétique)</term>
<term>Sous-type H1N1 du virus de la grippe A (immunologie)</term>
<term>Sous-type H1N1 du virus de la grippe A (pathogénicité)</term>
<term>Séquençage par oligonucléotides en batterie</term>
<term>Taux de survie</term>
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<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Chemokines</term>
<term>Cytokines</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term>
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<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Influenza, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Grippe humaine</term>
<term>Immunité innée</term>
<term>Macaca fascicularis</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Immunity, Innate</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza, Human</term>
<term>Macaca fascicularis</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Poumon</term>
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<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term>
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<keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Chimiokines</term>
<term>Cytokines</term>
<term>Grippe humaine</term>
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<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Grippe humaine</term>
<term>Macaca fascicularis</term>
<term>Poumon</term>
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<term>Lung</term>
<term>Macaca fascicularis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Survival Rate</term>
<term>Time Factors</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Animaux</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Régulation de l'expression des gènes</term>
<term>Réplication virale</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Séquençage par oligonucléotides en batterie</term>
<term>Taux de survie</term>
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<front><div type="abstract" xml:lang="en">The 1918 influenza pandemic was unusually severe, resulting in about 50 million deaths worldwide. The 1918 virus is also highly pathogenic in mice, and studies have identified a multigenic origin of this virulent phenotype in mice. However, these initial characterizations of the 1918 virus did not address the question of its pathogenic potential in primates. Here we demonstrate that the 1918 virus caused a highly pathogenic respiratory infection in a cynomolgus macaque model that culminated in acute respiratory distress and a fatal outcome. Furthermore, infected animals mounted an immune response, characterized by dysregulation of the antiviral response, that was insufficient for protection, indicating that atypical host innate immune responses may contribute to lethality. The ability of influenza viruses to modulate host immune responses, such as that demonstrated for the avian H5N1 influenza viruses, may be a feature shared by the virulent influenza viruses.</div>
</front>
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