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

Identifieur interne : 002F16 ( Main/Exploration ); précédent : 002F15; suivant : 002F17

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 :

RBID : Pascal:09-0374920

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English descriptors

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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<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en">
<term>Murine hepatitis virus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr">
<term>Virus de l'hépatite murine</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr">
<term>Cellules tueuses naturelles</term>
<term>Lymphocytes T CD4+</term>
<term>Lymphocytes T CD8+</term>
<term>Système immunitaire</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en">
<term>CD4-Positive T-Lymphocytes</term>
<term>CD8-Positive T-Lymphocytes</term>
<term>Immune System</term>
<term>Killer Cells, Natural</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr">
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Animals</term>
<term>Immunity</term>
<term>Mice</term>
<term>Mice, Inbred Strains</term>
<term>Species Specificity</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Animaux</term>
<term>Immunité</term>
<term>Interféron de type I</term>
<term>Lignées consanguines de souris</term>
<term>Réplication virale</term>
<term>Souris</term>
<term>Prévention</term>
<term>Réponse immune</term>
<term>Animal</term>
<term>Hépatite</term>
<term>Spécificité d'espèce</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<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>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>États-Unis</li>
</country>
<region>
<li>Iowa</li>
</region>
<settlement>
<li>Iowa City</li>
</settlement>
<orgName>
<li>Université de l'Iowa</li>
</orgName>
</list>
<tree>
<country name="États-Unis">
<region name="Iowa">
<name sortKey="Khanolkar, Aaruni" sort="Khanolkar, Aaruni" uniqKey="Khanolkar A" first="Aaruni" last="Khanolkar">Aaruni Khanolkar</name>
</region>
<name sortKey="Epping, Lecia L" sort="Epping, Lecia L" uniqKey="Epping L" first="Lecia L." last="Epping">Lecia L. Epping</name>
<name sortKey="Haag, Brayton A" sort="Haag, Brayton A" uniqKey="Haag B" first="Brayton A." last="Haag">Brayton A. Haag</name>
<name sortKey="Haring, Jodie S" sort="Haring, Jodie S" uniqKey="Haring J" first="Jodie S." last="Haring">Jodie S. Haring</name>
<name sortKey="Hartwig, Stacey M" sort="Hartwig, Stacey M" uniqKey="Hartwig S" first="Stacey M." last="Hartwig">Stacey M. Hartwig</name>
<name sortKey="Harty, John T" sort="Harty, John T" uniqKey="Harty J" first="John T." last="Harty">John T. Harty</name>
<name sortKey="Harty, John T" sort="Harty, John T" uniqKey="Harty J" first="John T." last="Harty">John T. Harty</name>
<name sortKey="Meyerholz, David K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K." last="Meyerholz">David K. Meyerholz</name>
<name sortKey="Varga, Steven M" sort="Varga, Steven M" uniqKey="Varga S" first="Steven M." last="Varga">Steven M. Varga</name>
<name sortKey="Varga, Steven M" sort="Varga, Steven M" uniqKey="Varga S" first="Steven M." last="Varga">Steven M. Varga</name>
</country>
</tree>
</affiliations>
</record>

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