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1918 pandemic influenza virus and Streptococcus pneumoniae co-infection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans.

Identifieur interne : 001A85 ( Ncbi/Curation ); précédent : 001A84; suivant : 001A86

1918 pandemic influenza virus and Streptococcus pneumoniae co-infection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans.

Auteurs : Kathie-Anne Walters [États-Unis] ; Felice D'Agnillo [États-Unis] ; Zong-Mei Sheng [États-Unis] ; Jason Kindrachuk [États-Unis] ; Louis M. Schwartzman [États-Unis] ; Rolf E. Kuestner [États-Unis] ; Daniel S. Chertow [États-Unis] ; Basil T. Golding [États-Unis] ; Jeffery K. Taubenberger [États-Unis] ; John C. Kash [États-Unis]

Source :

RBID : pubmed:26383585

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English descriptors

Abstract

To study bacterial co-infection following 1918 H1N1 influenza virus infection, mice were inoculated with the 1918 influenza virus, followed by Streptococcus pneumoniae (SP) 72 h later. Co-infected mice exhibited markedly more severe disease, shortened survival time and more severe lung pathology, including widespread thrombi. Transcriptional profiling revealed activation of coagulation only in co-infected mice, consistent with the extensive thrombogenesis observed. Immunohistochemistry showed extensive expression of tissue factor (F3) and prominent deposition of neutrophil elastase on endothelial and epithelial cells in co-infected mice. Lung sections of SP-positive 1918 autopsy cases showed extensive thrombi and prominent staining for F3 in alveolar macrophages, monocytes, neutrophils, endothelial and epithelial cells, in contrast to co-infection-positive 2009 pandemic H1N1 autopsy cases. This study reveals that a distinctive feature of 1918 influenza virus and SP co-infection in mice and humans is extensive expression of tissue factor and activation of the extrinsic coagulation pathway leading to widespread pulmonary thrombosis.

DOI: 10.1002/path.4638
PubMed: 26383585

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Le document en format XML

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<term>Blood Coagulation</term>
<term>Coinfection (complications)</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Humans</term>
<term>Immunohistochemistry</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza Pandemic, 1918-1919</term>
<term>Influenza, Human (complications)</term>
<term>Influenza, Human (microbiology)</term>
<term>Influenza, Human (pathology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Orthomyxoviridae Infections (complications)</term>
<term>Orthomyxoviridae Infections (microbiology)</term>
<term>Orthomyxoviridae Infections (pathology)</term>
<term>Pneumococcal Infections (complications)</term>
<term>Pneumococcal Infections (microbiology)</term>
<term>Pneumococcal Infections (pathology)</term>
<term>Pulmonary Embolism (microbiology)</term>
<term>Pulmonary Embolism (pathology)</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Streptococcus pneumoniae</term>
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<term>Animaux</term>
<term>Co-infection ()</term>
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<term>Embolie pulmonaire (microbiologie)</term>
<term>Femelle</term>
<term>Grippe humaine ()</term>
<term>Grippe humaine (anatomopathologie)</term>
<term>Grippe humaine (microbiologie)</term>
<term>Humains</term>
<term>Immunohistochimie</term>
<term>Infections à Orthomyxoviridae ()</term>
<term>Infections à Orthomyxoviridae (anatomopathologie)</term>
<term>Infections à Orthomyxoviridae (microbiologie)</term>
<term>Infections à pneumocoques ()</term>
<term>Infections à pneumocoques (anatomopathologie)</term>
<term>Infections à pneumocoques (microbiologie)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Pandémie de grippe de 1918-1919</term>
<term>RT-PCR</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
<term>Streptococcus pneumoniae</term>
<term>Séquençage par oligonucléotides en batterie</term>
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<term>Embolie pulmonaire</term>
<term>Grippe humaine</term>
<term>Infections à Orthomyxoviridae</term>
<term>Infections à pneumocoques</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en">
<term>Coinfection</term>
<term>Influenza, Human</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumococcal Infections</term>
</keywords>
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<term>Embolie pulmonaire</term>
<term>Grippe humaine</term>
<term>Infections à Orthomyxoviridae</term>
<term>Infections à pneumocoques</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en">
<term>Influenza, Human</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumococcal Infections</term>
<term>Pulmonary Embolism</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Influenza, Human</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumococcal Infections</term>
<term>Pulmonary Embolism</term>
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<term>Blood Coagulation</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Humans</term>
<term>Immunohistochemistry</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza Pandemic, 1918-1919</term>
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<term>Mice, Inbred BALB C</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Streptococcus pneumoniae</term>
</keywords>
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<term>Animaux</term>
<term>Co-infection</term>
<term>Coagulation sanguine</term>
<term>Femelle</term>
<term>Grippe humaine</term>
<term>Humains</term>
<term>Immunohistochimie</term>
<term>Infections à Orthomyxoviridae</term>
<term>Infections à pneumocoques</term>
<term>Modèles animaux de maladie humaine</term>
<term>Pandémie de grippe de 1918-1919</term>
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<term>Souris de lignée BALB C</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
<term>Streptococcus pneumoniae</term>
<term>Séquençage par oligonucléotides en batterie</term>
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<front>
<div type="abstract" xml:lang="en">To study bacterial co-infection following 1918 H1N1 influenza virus infection, mice were inoculated with the 1918 influenza virus, followed by Streptococcus pneumoniae (SP) 72 h later. Co-infected mice exhibited markedly more severe disease, shortened survival time and more severe lung pathology, including widespread thrombi. Transcriptional profiling revealed activation of coagulation only in co-infected mice, consistent with the extensive thrombogenesis observed. Immunohistochemistry showed extensive expression of tissue factor (F3) and prominent deposition of neutrophil elastase on endothelial and epithelial cells in co-infected mice. Lung sections of SP-positive 1918 autopsy cases showed extensive thrombi and prominent staining for F3 in alveolar macrophages, monocytes, neutrophils, endothelial and epithelial cells, in contrast to co-infection-positive 2009 pandemic H1N1 autopsy cases. This study reveals that a distinctive feature of 1918 influenza virus and SP co-infection in mice and humans is extensive expression of tissue factor and activation of the extrinsic coagulation pathway leading to widespread pulmonary thrombosis.</div>
</front>
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