SrasV1, PubMed, Checkpoint, bibRecord, 002096

Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice.

Identifieur interne : 002096 ( PubMed/Checkpoint ); précédent : 002095; suivant : 002097

Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice.

Auteurs : Nadine De Albuquerque [Canada] ; Ehtesham Baig ; Xuezhong Ma ; Jianhua Zhang ; William He ; Andrea Rowe ; Marlena Habal ; Mingfeng Liu ; Itay Shalev ; Gregory P. Downey ; Reginald Gorczynski ; Jagdish Butany ; Julian Leibowitz ; Susan R. Weiss ; Ian D. Mcgilvray ; M James Phillips ; Eleanor N. Fish ; Gary A. Levy

Source :

Journal of virology [ 0022-538X ] ; 2006.

RBID : pubmed:17041219

Descripteurs français

KwdFr :
- ADN complémentaire (génétique), ARN messager (génétique), ARN messager (métabolisme), Animaux, Cytokines (génétique), Cytokines (métabolisme), Femelle, Humains, Infections à coronavirus (anatomopathologie), Infections à coronavirus (génétique), Infections à coronavirus (immunologie), Infections à coronavirus (étiologie), Interférons (génétique), Interférons (métabolisme), Microscopie électronique, Modèles animaux de maladie humaine, Poumon (anatomopathologie), Poumon (virologie), Souris, Souris de lignée A, Souris de lignée BALB C, Souris de lignée C3H, Souris de lignée C57BL, Spécificité d'espèce, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (étiologie), Séquence nucléotidique, Virus de l'hépatite murine (), Virus de l'hépatite murine (immunologie), Virus de l'hépatite murine (pathogénicité).
MESH :
- anatomopathologie : Infections à coronavirus, Poumon, Syndrome respiratoire aigu sévère.
- génétique : ADN complémentaire, ARN messager, Cytokines, Infections à coronavirus, Interférons, Syndrome respiratoire aigu sévère.
- immunologie : Infections à coronavirus, Syndrome respiratoire aigu sévère, Virus de l'hépatite murine.
- métabolisme : ARN messager, Cytokines, Interférons.
- pathogénicité : Virus de l'hépatite murine.
- virologie : Poumon.
- étiologie : Infections à coronavirus, Syndrome respiratoire aigu sévère.
- Animaux, Femelle, Humains, Microscopie électronique, Modèles animaux de maladie humaine, Souris, Souris de lignée A, Souris de lignée BALB C, Souris de lignée C3H, Souris de lignée C57BL, Spécificité d'espèce, Séquence nucléotidique, Virus de l'hépatite murine.

English descriptors

KwdEn :
- Animals, Base Sequence, Coronavirus Infections (etiology), Coronavirus Infections (genetics), Coronavirus Infections (immunology), Coronavirus Infections (pathology), Cytokines (genetics), Cytokines (metabolism), DNA, Complementary (genetics), Disease Models, Animal, Female, Humans, Interferons (genetics), Interferons (metabolism), Lung (pathology), Lung (virology), Mice, Mice, Inbred A, Mice, Inbred BALB C, Mice, Inbred C3H, Mice, Inbred C57BL, Microscopy, Electron, Murine hepatitis virus (classification), Murine hepatitis virus (immunology), Murine hepatitis virus (pathogenicity), RNA, Messenger (genetics), RNA, Messenger (metabolism), Severe Acute Respiratory Syndrome (etiology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Species Specificity.
MESH :
- chemical , genetics : Cytokines, DNA, Complementary, Interferons, RNA, Messenger.
- classification : Murine hepatitis virus.
- etiology : Coronavirus Infections, Severe Acute Respiratory Syndrome.
- genetics : Coronavirus Infections, Severe Acute Respiratory Syndrome.
- immunology : Coronavirus Infections, Murine hepatitis virus, Severe Acute Respiratory Syndrome.
- chemical , metabolism : Cytokines, Interferons, RNA, Messenger.
- pathogenicity : Murine hepatitis virus.
- pathology : Coronavirus Infections, Lung, Severe Acute Respiratory Syndrome.
- virology : Lung.
- Animals, Base Sequence, Disease Models, Animal, Female, Humans, Mice, Mice, Inbred A, Mice, Inbred BALB C, Mice, Inbred C3H, Mice, Inbred C57BL, Microscopy, Electron, Species Specificity.

Abstract

Severe acute respiratory syndrome (SARS) is a life-threatening infectious disease which has been difficult to study and treat because of the lack of a readily available animal model. Intranasal infection of A/J mice with the coronavirus murine hepatitis virus strain 1 (MHV-1) produced pulmonary pathological features of SARS. All MHV-1-infected A/J mice developed progressive interstitial pneumonitis, including dense macrophage infiltrates, giant cells, and hyaline membranes, resulting in death of all animals. In contrast, other mouse strains developed only mild transitory disease. Infected A/J mice had significantly higher cytokine levels, particularly macrophage chemoattractant protein 1 (MCP-1/CCL-2), gamma interferon, and tumor necrosis factor alpha. Furthermore, FGL2/fibroleukin mRNA transcripts and protein and fibrin deposits were markedly increased in the lungs of infected A/J mice. These animals developed a less robust type I interferon response to MHV-1 infection than resistant C57BL/6J mice, and treatment with recombinant beta interferon improved survival. This study describes a potentially useful small animal model of human SARS, defines its pathogenesis, and suggests treatment strategies.

DOI: 10.1128/JVI.00747-06
PubMed: 17041219

Affiliations:

Canada

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to stream PubMed, to step Curation: 002017

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pubmed:17041219

Le document en format XML

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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is a life-threatening infectious disease which has been difficult to study and treat because of the lack of a readily available animal model. Intranasal infection of A/J mice with the coronavirus murine hepatitis virus strain 1 (MHV-1) produced pulmonary pathological features of SARS. All MHV-1-infected A/J mice developed progressive interstitial pneumonitis, including dense macrophage infiltrates, giant cells, and hyaline membranes, resulting in death of all animals. In contrast, other mouse strains developed only mild transitory disease. Infected A/J mice had significantly higher cytokine levels, particularly macrophage chemoattractant protein 1 (MCP-1/CCL-2), gamma interferon, and tumor necrosis factor alpha. Furthermore, FGL2/fibroleukin mRNA transcripts and protein and fibrin deposits were markedly increased in the lungs of infected A/J mice. These animals developed a less robust type I interferon response to MHV-1 infection than resistant C57BL/6J mice, and treatment with recombinant beta interferon improved survival. This study describes a potentially useful small animal model of human SARS, defines its pathogenesis, and suggests treatment strategies.</div>
</front>
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<DateCompleted><Year>2006</Year>
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<ArticleTitle>Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice.</ArticleTitle>
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<Abstract><AbstractText>Severe acute respiratory syndrome (SARS) is a life-threatening infectious disease which has been difficult to study and treat because of the lack of a readily available animal model. Intranasal infection of A/J mice with the coronavirus murine hepatitis virus strain 1 (MHV-1) produced pulmonary pathological features of SARS. All MHV-1-infected A/J mice developed progressive interstitial pneumonitis, including dense macrophage infiltrates, giant cells, and hyaline membranes, resulting in death of all animals. In contrast, other mouse strains developed only mild transitory disease. Infected A/J mice had significantly higher cytokine levels, particularly macrophage chemoattractant protein 1 (MCP-1/CCL-2), gamma interferon, and tumor necrosis factor alpha. Furthermore, FGL2/fibroleukin mRNA transcripts and protein and fibrin deposits were markedly increased in the lungs of infected A/J mice. These animals developed a less robust type I interferon response to MHV-1 infection than resistant C57BL/6J mice, and treatment with recombinant beta interferon improved survival. This study describes a potentially useful small animal model of human SARS, defines its pathogenesis, and suggests treatment strategies.</AbstractText>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>De Albuquerque</LastName>
<ForeName>Nadine</ForeName>
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<AffiliationInfo><Affiliation>Toronto General Hospital, 585 University Ave., NCSB-11-1236, Toronto, Ontario M5G 2N2, Canada.</Affiliation>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Jianhua</ForeName>
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<Author ValidYN="Y"><LastName>He</LastName>
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<Author ValidYN="Y"><LastName>Downey</LastName>
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Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice.

Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice.

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