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 : 000438Murine 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. LevySource :
- Journal of virology [ 0022-538X ] ; 2006.
Descripteurs français
- Pascal (Inist)
English descriptors
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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.
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NO : | PASCAL 06-0518531 INIST |
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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:06-0518531Le document en format XML
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</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">06-0518531</idno>
<date when="2006">2006</date>
<idno type="stanalyst">PASCAL 06-0518531 INIST</idno>
<idno type="RBID">Pascal:06-0518531</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000437</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><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>
<author><name sortKey="De Albuquerque, Nadine" sort="De Albuquerque, Nadine" uniqKey="De Albuquerque N" first="Nadine" last="De Albuquerque">Nadine De Albuquerque</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Medicine, University Health Network</s1>
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<affiliation><inist:fA14 i1="02"><s1>the Multi Organ Transplant Program, University Health Network</s1>
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</author>
<author><name sortKey="Baig, Ehtesham" sort="Baig, Ehtesham" uniqKey="Baig E" first="Ehtesham" last="Baig">Ehtesham Baig</name>
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</affiliation>
</author>
<author><name sortKey="Xuezhong Ma" sort="Xuezhong Ma" uniqKey="Xuezhong Ma" last="Xuezhong Ma">XUEZHONG MA</name>
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<affiliation><inist:fA14 i1="02"><s1>the Multi Organ Transplant Program, University Health Network</s1>
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</author>
<author><name sortKey="Jianhua Zhang" sort="Jianhua Zhang" uniqKey="Jianhua Zhang" last="Jianhua Zhang">JIANHUA ZHANG</name>
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</author>
<author><name sortKey="He, William" sort="He, William" uniqKey="He W" first="William" last="He">William He</name>
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</affiliation>
</author>
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</affiliation>
</author>
<author><name sortKey="Mingfeng Liu" sort="Mingfeng Liu" uniqKey="Mingfeng Liu" last="Mingfeng Liu">MINGFENG LIU</name>
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<author><name sortKey="Downey, Gregory P" sort="Downey, Gregory P" uniqKey="Downey G" first="Gregory P." last="Downey">Gregory P. Downey</name>
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<author><name sortKey="Gorczynski, Reginald" sort="Gorczynski, Reginald" uniqKey="Gorczynski R" first="Reginald" last="Gorczynski">Reginald Gorczynski</name>
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</analytic>
<series><title level="j" type="main">Journal of virology</title>
<title level="j" type="abbreviated">J. virol.</title>
<idno type="ISSN">0022-538X</idno>
<imprint><date when="2006">2006</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Journal of virology</title>
<title level="j" type="abbreviated">J. virol.</title>
<idno type="ISSN">0022-538X</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Hepatitis A virus</term>
<term>Microbiology</term>
<term>Models</term>
<term>Mouse</term>
<term>Murine hepatitis virus</term>
<term>Severe acute respiratory syndrome</term>
<term>Strain</term>
<term>Virology</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Virus hépatite murine</term>
<term>Virus hépatite A</term>
<term>Souris</term>
<term>Souche</term>
<term>Modèle</term>
<term>Microbiologie</term>
<term>Virologie</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<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>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-538X</s0>
</fA01>
<fA03 i2="1"><s0>J. virol.</s0>
</fA03>
<fA05><s2>80</s2>
</fA05>
<fA06><s2>21</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>DE ALBUQUERQUE (Nadine)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>BAIG (Ehtesham)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>XUEZHONG MA</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>JIANHUA ZHANG</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>HE (William)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>ROWE (Andrea)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>HABAL (Marlena)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>MINGFENG LIU</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>SHALEV (Itay)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>DOWNEY (Gregory P.)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>GORCZYNSKI (Reginald)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>BUTANY (Jagdish)</s1>
</fA11>
<fA11 i1="13" i2="1"><s1>LEIBOWITZ (Julian)</s1>
</fA11>
<fA11 i1="14" i2="1"><s1>WEISS (Susan R.)</s1>
</fA11>
<fA11 i1="15" i2="1"><s1>MCGILVRAY (Ian D.)</s1>
</fA11>
<fA11 i1="16" i2="1"><s1>PHILLIPS (M. James)</s1>
</fA11>
<fA11 i1="17" i2="1"><s1>FISH (Eleanor N.)</s1>
</fA11>
<fA11 i1="18" i2="1"><s1>LEVY (Gary A.)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Medicine, University Health Network</s1>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>18 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>the Multi Organ Transplant Program, University Health Network</s1>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>18 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>University of Toronto</s1>
<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Surgery, University Health Network</s1>
<s3>CAN</s3>
<sZ>11 aut.</sZ>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Pathology, University Health Network</s1>
<s3>CAN</s3>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department of Microbial and Molecular Pathogenesis, Texas A&M University System- HSC</s1>
<s2>College Station, Texas</s2>
<s3>USA</s3>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Department of Microbiology, University of Pennsylvania</s1>
<s2>Philadelphia, Pennsylvania</s2>
<s3>USA</s3>
<sZ>14 aut.</sZ>
</fA14>
<fA20><s1>10382-10394</s1>
</fA20>
<fA21><s1>2006</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>13592</s2>
<s5>354000158805950100</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2006 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>58 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>06-0518531</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Journal of virology</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A05C10</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Virus hépatite murine</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Murine hepatitis virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Murine hepatitis virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Virus hépatite A</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Hepatitis A virus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Hepatitis A virus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Souris</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Mouse</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Ratón</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Souche</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Strain</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Cepa</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Modèle</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Models</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Modelo</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Microbiologie</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Microbiology</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Microbiología</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Virologie</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Virology</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Virología</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Hepatovirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Hepatovirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Hepatovirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Picornaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Picornaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Picornaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="12" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="12" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="12" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="13" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="13" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="13" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>338</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 06-0518531 INIST</NO>
<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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