SrasV1, PascalFrancis, Curation, bibRecord, 000796

Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome

Identifieur interne : 000796 ( PascalFrancis/Curation ); précédent : 000795; suivant : 000797

Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome

Auteurs : Aaruni Khanolkar [États-Unis] ; Stacey M. Hartwig [États-Unis] ; Brayton A. Haag [États-Unis] ; David K. Meyerholz [États-Unis] ; Lecia L. Epping [États-Unis] ; Jodie S. Haring [États-Unis] ; Steven M. Varga [États-Unis] ; John T. Harty [États-Unis]

Source :

Journal of virology [ 0022-538X ] ; 2009.

RBID : Pascal:09-0374920

Descripteurs français

Pascal (Inist)
- Souris, Prévention, Réponse immune, Animal, Hépatite, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Animal, Hepatitis, Immune response, Mouse, Prevention, Severe acute respiratory syndrome.

Abstract

Intranasal mouse hepatitis virus type 1 (MHV-1) infection of mice induces lung pathology similar to that observed in severe acute respiratory syndrome (SARS) patients. However, the severity of MHV-1-induced pulmonary disease varies among mouse strains, and it has been suggested that differences in the host immune response might account for this variation. It has also been suggested that immunopathology may represent an important clinical feature of SARS. Little is known about the host immune response to MHV-1 and how it might contribute to some of the pathological changes detected in infected mice. In this study we show that an intact type I interferon system and the adaptive immune responses are required for controlling MHV-1 replication and preventing morbidity and mortality in resistant C57BL/6J mice after infection. The NK cell response also helps minimize the severity of illness following MHV-1 infection of C57BL/6J mice. In A/J and C3H/HeJ mice, which are highly susceptible to MHV-1-induced disease, we demonstrate that both CD4 and CD8 T cells contribute to morbidity during primary infection, and memory responses can enhance morbidity and mortality during subsequent reexposure to MHV-1. However, morbidity in A/J and C3H/HeJ mice can be minimized by treating them with immune serum prior to MHV-1 infection. Overall, our findings highlight the role of the host immune response in contributing to the pathogenesis of coronavirus-induced respiratory disease.

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A11	`02`	`1`		`@1 HARTWIG (Stacey M.)`
A11	`03`	`1`		`@1 HAAG (Brayton A.)`
A11	`04`	`1`		`@1 MEYERHOLZ (David K.)`
A11	`05`	`1`		`@1 EPPING (Lecia L.)`
A11	`06`	`1`		`@1 HARING (Jodie S.)`
A11	`07`	`1`		`@1 VARGA (Steven M.)`
A11	`08`	`1`		`@1 HARTY (John T.)`
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C01	`01`		`ENG`	@0 Intranasal mouse hepatitis virus type 1 (MHV-1) infection of mice induces lung pathology similar to that observed in severe acute respiratory syndrome (SARS) patients. However, the severity of MHV-1-induced pulmonary disease varies among mouse strains, and it has been suggested that differences in the host immune response might account for this variation. It has also been suggested that immunopathology may represent an important clinical feature of SARS. Little is known about the host immune response to MHV-1 and how it might contribute to some of the pathological changes detected in infected mice. In this study we show that an intact type I interferon system and the adaptive immune responses are required for controlling MHV-1 replication and preventing morbidity and mortality in resistant C57BL/6J mice after infection. The NK cell response also helps minimize the severity of illness following MHV-1 infection of C57BL/6J mice. In A/J and C3H/HeJ mice, which are highly susceptible to MHV-1-induced disease, we demonstrate that both CD4 and CD8 T cells contribute to morbidity during primary infection, and memory responses can enhance morbidity and mortality during subsequent reexposure to MHV-1. However, morbidity in A/J and C3H/HeJ mice can be minimized by treating them with immune serum prior to MHV-1 infection. Overall, our findings highlight the role of the host immune response in contributing to the pathogenesis of coronavirus-induced respiratory disease.
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C07	`04`	`X`	`FRE`	`@0 Pathologie de l'appareil digestif @5 13`
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N21				`@1 271`
N44	`01`			`@1 OTO`
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Le document en format XML

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<series><title level="j" type="main">Journal of virology</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Souris</term>
<term>Prévention</term>
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<front><div type="abstract" xml:lang="en">Intranasal mouse hepatitis virus type 1 (MHV-1) infection of mice induces lung pathology similar to that observed in severe acute respiratory syndrome (SARS) patients. However, the severity of MHV-1-induced pulmonary disease varies among mouse strains, and it has been suggested that differences in the host immune response might account for this variation. It has also been suggested that immunopathology may represent an important clinical feature of SARS. Little is known about the host immune response to MHV-1 and how it might contribute to some of the pathological changes detected in infected mice. In this study we show that an intact type I interferon system and the adaptive immune responses are required for controlling MHV-1 replication and preventing morbidity and mortality in resistant C57BL/6J mice after infection. The NK cell response also helps minimize the severity of illness following MHV-1 infection of C57BL/6J mice. In A/J and C3H/HeJ mice, which are highly susceptible to MHV-1-induced disease, we demonstrate that both CD4 and CD8 T cells contribute to morbidity during primary infection, and memory responses can enhance morbidity and mortality during subsequent reexposure to MHV-1. However, morbidity in A/J and C3H/HeJ mice can be minimized by treating them with immune serum prior to MHV-1 infection. Overall, our findings highlight the role of the host immune response in contributing to the pathogenesis of coronavirus-induced respiratory disease.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>KHANOLKAR (Aaruni)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>HARTWIG (Stacey M.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>HAAG (Brayton A.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>MEYERHOLZ (David K.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>EPPING (Lecia L.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>HARING (Jodie S.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>VARGA (Steven M.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>HARTY (John T.)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Microbiology, University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Interdisciplinary Graduate Program in Immunology University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Pathology, University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA20><s1>9258-9272</s1>
</fA20>
<fA21><s1>2009</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>13592</s2>
<s5>354000171848630230</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2009 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>89 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>09-0374920</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>Intranasal mouse hepatitis virus type 1 (MHV-1) infection of mice induces lung pathology similar to that observed in severe acute respiratory syndrome (SARS) patients. However, the severity of MHV-1-induced pulmonary disease varies among mouse strains, and it has been suggested that differences in the host immune response might account for this variation. It has also been suggested that immunopathology may represent an important clinical feature of SARS. Little is known about the host immune response to MHV-1 and how it might contribute to some of the pathological changes detected in infected mice. In this study we show that an intact type I interferon system and the adaptive immune responses are required for controlling MHV-1 replication and preventing morbidity and mortality in resistant C57BL/6J mice after infection. The NK cell response also helps minimize the severity of illness following MHV-1 infection of C57BL/6J mice. In A/J and C3H/HeJ mice, which are highly susceptible to MHV-1-induced disease, we demonstrate that both CD4 and CD8 T cells contribute to morbidity during primary infection, and memory responses can enhance morbidity and mortality during subsequent reexposure to MHV-1. However, morbidity in A/J and C3H/HeJ mice can be minimized by treating them with immune serum prior to MHV-1 infection. Overall, our findings highlight the role of the host immune response in contributing to the pathogenesis of coronavirus-induced respiratory disease.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A05C10</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Souris</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Mouse</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Ratón</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Prévention</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Prevention</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Prevención</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Réponse immune</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Immune response</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Respuesta inmune</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Animal</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Animal</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Animal</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Hépatite</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Hepatitis</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Hepatitis</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="06" 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>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie de l'appareil digestif</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Digestive diseases</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Aparato digestivo patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Pathologie du foie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Hepatic disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Hígado patología</s0>
<s5>16</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Pathologie de l'appareil respiratoire</s0>
<s5>17</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>17</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>17</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Pathologie des poumons</s0>
<s5>18</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>18</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>18</s5>
</fC07>
<fN21><s1>271</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome

Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome

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