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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 : 000603 ( PubMed/Curation ); précédent : 000602; suivant : 000604

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 :

The Journal of pathology [ 1096-9896 ] ; 2016.

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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<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>
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<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>Embolie pulmonaire (anatomopathologie)</term>
<term>Embolie pulmonaire (microbiologie)</term>
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<term>Grippe humaine ()</term>
<term>Grippe humaine (anatomopathologie)</term>
<term>Grippe humaine (microbiologie)</term>
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<term>Infections à Orthomyxoviridae (anatomopathologie)</term>
<term>Infections à Orthomyxoviridae (microbiologie)</term>
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<term>Infections à pneumocoques</term>
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<term>Orthomyxoviridae Infections</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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<ArticleTitle>1918 pandemic influenza virus and Streptococcus pneumoniae co-infection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans.</ArticleTitle>
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<Abstract><AbstractText>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.</AbstractText>
<CopyrightInformation>Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Walters</LastName>
<ForeName>Kathie-Anne</ForeName>
<Initials>KA</Initials>
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</AffiliationInfo>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Sheng</LastName>
<ForeName>Zong-Mei</ForeName>
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<AffiliationInfo><Affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, 20892, USA.</Affiliation>
</AffiliationInfo>
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<ForeName>Jason</ForeName>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Schwartzman</LastName>
<ForeName>Louis M</ForeName>
<Initials>LM</Initials>
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</AffiliationInfo>
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<ForeName>Rolf E</ForeName>
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</AffiliationInfo>
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</AffiliationInfo>
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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.

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

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