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

Identifieur interne : 000437 ( PascalFrancis/Corpus ); précédent : 000436; suivant : 000438

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

Auteurs : Nadine De Albuquerque ; 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 :

RBID : Pascal:06-0518531

Descripteurs français

English descriptors

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11 08  1    @1 MINGFENG LIU
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Format Inist (serveur)

NO : PASCAL 06-0518531 INIST
ET : Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice
AU : DE ALBUQUERQUE (Nadine); BAIG (Ehtesham); XUEZHONG MA; JIANHUA ZHANG; HE (William); ROWE (Andrea); HABAL (Marlena); MINGFENG LIU; SHALEV (Itay); DOWNEY (Gregory P.); GORCZYNSKI (Reginald); BUTANY (Jagdish); LEIBOWITZ (Julian); WEISS (Susan R.); MCGILVRAY (Ian D.); PHILLIPS (M. James); FISH (Eleanor N.); LEVY (Gary A.)
AF : Department of Medicine, University Health Network/Canada (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut., 10 aut., 18 aut.); the Multi Organ Transplant Program, University Health Network/Canada (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut., 10 aut., 11 aut., 15 aut., 16 aut., 18 aut.); University of Toronto/Toronto, Ontario/Canada (2 aut., 15 aut., 17 aut., 18 aut.); Surgery, University Health Network/Canada (11 aut., 15 aut.); Pathology, University Health Network/Canada (12 aut., 16 aut.); Department of Microbial and Molecular Pathogenesis, Texas A&M University System- HSC/College Station, Texas/Etats-Unis (13 aut.); Department of Microbiology, University of Pennsylvania/Philadelphia, Pennsylvania/Etats-Unis (14 aut.)
DT : Publication en série; Niveau analytique
SO : Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2006; Vol. 80; No. 21; Pp. 10382-10394; Bibl. 58 ref.
LA : Anglais
EA : 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.
CC : 002A05C10
FD : Virus hépatite murine; Virus hépatite A; Souris; Souche; Modèle; Microbiologie; Virologie; Syndrome respiratoire aigu sévère
FG : Coronavirus; Coronaviridae; Nidovirales; Virus; Hepatovirus; Picornaviridae; Rodentia; Mammalia; Vertebrata; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED : Murine hepatitis virus; Hepatitis A virus; Mouse; Strain; Models; Microbiology; Virology; Severe acute respiratory syndrome
EG : Coronavirus; Coronaviridae; Nidovirales; Virus; Hepatovirus; Picornaviridae; Rodentia; Mammalia; Vertebrata; Respiratory disease; Viral disease; Infection; Lung disease
SD : Murine hepatitis virus; Hepatitis A virus; Ratón; Cepa; Modelo; Microbiología; Virología; Síndrome respiratorio agudo severo
LO : INIST-13592.354000158805950100
ID : 06-0518531

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Pascal:06-0518531

Le document en format XML

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<title xml:lang="en" level="a">Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice</title>
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<title level="j" type="main">Journal of virology</title>
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<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>
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<s0>Infección</s0>
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<s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
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<s0>Lung disease</s0>
<s5>16</s5>
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<s0>Pulmón patología</s0>
<s5>16</s5>
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<ET>Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice</ET>
<AU>DE ALBUQUERQUE (Nadine); BAIG (Ehtesham); XUEZHONG MA; JIANHUA ZHANG; HE (William); ROWE (Andrea); HABAL (Marlena); MINGFENG LIU; SHALEV (Itay); DOWNEY (Gregory P.); GORCZYNSKI (Reginald); BUTANY (Jagdish); LEIBOWITZ (Julian); WEISS (Susan R.); MCGILVRAY (Ian D.); PHILLIPS (M. James); FISH (Eleanor N.); LEVY (Gary A.)</AU>
<AF>Department of Medicine, University Health Network/Canada (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut., 10 aut., 18 aut.); the Multi Organ Transplant Program, University Health Network/Canada (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut., 10 aut., 11 aut., 15 aut., 16 aut., 18 aut.); University of Toronto/Toronto, Ontario/Canada (2 aut., 15 aut., 17 aut., 18 aut.); Surgery, University Health Network/Canada (11 aut., 15 aut.); Pathology, University Health Network/Canada (12 aut., 16 aut.); Department of Microbial and Molecular Pathogenesis, Texas A&M University System- HSC/College Station, Texas/Etats-Unis (13 aut.); Department of Microbiology, University of Pennsylvania/Philadelphia, Pennsylvania/Etats-Unis (14 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2006; Vol. 80; No. 21; Pp. 10382-10394; Bibl. 58 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002A05C10</CC>
<FD>Virus hépatite murine; Virus hépatite A; Souris; Souche; Modèle; Microbiologie; Virologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronavirus; Coronaviridae; Nidovirales; Virus; Hepatovirus; Picornaviridae; Rodentia; Mammalia; Vertebrata; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG>
<ED>Murine hepatitis virus; Hepatitis A virus; Mouse; Strain; Models; Microbiology; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronavirus; Coronaviridae; Nidovirales; Virus; Hepatovirus; Picornaviridae; Rodentia; Mammalia; Vertebrata; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Murine hepatitis virus; Hepatitis A virus; Ratón; Cepa; Modelo; Microbiología; Virología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13592.354000158805950100</LO>
<ID>06-0518531</ID>
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