Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome▿
Identifieur interne : 001F59 ( Ncbi/Merge ); précédent : 001F58; suivant : 001F60Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome▿
Auteurs : Aaruni Khanolkar ; Stacey M. Hartwig ; Brayton A. Haag ; David K. Meyerholz ; Lecia L. Epping ; Jodie S. Haring ; Steven M. Varga ; John T. HartySource :
- Journal of Virology [ 0022-538X ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Cellules tueuses naturelles (immunologie), Cellules tueuses naturelles (virologie), Immunité, Interféron de type I, Lignées consanguines de souris, Lymphocytes T CD4+ (virologie), Lymphocytes T CD8+ (virologie), Réplication virale, Souris, Spécificité d'espèce, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (étiologie), Système immunitaire (virologie), Virus de l'hépatite murine (immunologie), Virus de l'hépatite murine (pathogénicité).
- MESH :
- immunologie : Cellules tueuses naturelles, Syndrome respiratoire aigu sévère, Virus de l'hépatite murine.
- pathogénicité : Virus de l'hépatite murine.
- virologie : Cellules tueuses naturelles, Lymphocytes T CD4+, Lymphocytes T CD8+, Système immunitaire.
- étiologie : Syndrome respiratoire aigu sévère.
- Animaux, Immunité, Interféron de type I, Lignées consanguines de souris, Réplication virale, Souris, Spécificité d'espèce.
English descriptors
- KwdEn :
- Animals, CD4-Positive T-Lymphocytes (virology), CD8-Positive T-Lymphocytes (virology), Immune System (virology), Immunity, Interferon Type I, Killer Cells, Natural (immunology), Killer Cells, Natural (virology), Mice, Mice, Inbred Strains, Murine hepatitis virus (immunology), Murine hepatitis virus (pathogenicity), Severe Acute Respiratory Syndrome (etiology), Severe Acute Respiratory Syndrome (immunology), Species Specificity, Virus Replication.
- MESH :
- chemical : Interferon Type I.
- etiology : Severe Acute Respiratory Syndrome.
- immunology : Killer Cells, Natural, Murine hepatitis virus, Severe Acute Respiratory Syndrome.
- pathogenicity : Murine hepatitis virus.
- virology : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Immune System, Killer Cells, Natural.
- Animals, Immunity, Mice, Mice, Inbred Strains, Species Specificity, Virus Replication.
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.
Url:
DOI: 10.1128/JVI.00355-09
PubMed: 19570864
PubMed Central: 2738266
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PMC:2738266Le document en format XML
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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.</p></div></front></TEI><double pmid="19570864"><pmc><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome<xref ref-type="fn" rid="fn3">▿</xref> </title><author><name sortKey="Khanolkar, Aaruni" sort="Khanolkar, Aaruni" uniqKey="Khanolkar A" first="Aaruni" last="Khanolkar">Aaruni Khanolkar</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Hartwig, Stacey M" sort="Hartwig, Stacey M" uniqKey="Hartwig S" first="Stacey M." last="Hartwig">Stacey M. Hartwig</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Haag, Brayton A" sort="Haag, Brayton A" uniqKey="Haag B" first="Brayton A." last="Haag">Brayton A. Haag</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Meyerholz, David K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K." last="Meyerholz">David K. Meyerholz</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Epping, Lecia L" sort="Epping, Lecia L" uniqKey="Epping L" first="Lecia L." last="Epping">Lecia L. Epping</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Haring, Jodie S" sort="Haring, Jodie S" uniqKey="Haring J" first="Jodie S." last="Haring">Jodie S. Haring</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Varga, Steven M" sort="Varga, Steven M" uniqKey="Varga S" first="Steven M." last="Varga">Steven M. Varga</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Harty, John T" sort="Harty, John T" uniqKey="Harty J" first="John T." last="Harty">John T. Harty</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">19570864</idno><idno type="pmc">2738266</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738266</idno><idno type="RBID">PMC:2738266</idno><idno type="doi">10.1128/JVI.00355-09</idno><date when="2009">2009</date><idno type="wicri:Area/Pmc/Corpus">000C97</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000C97</idno><idno type="wicri:Area/Pmc/Curation">000C97</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000C97</idno><idno type="wicri:Area/Pmc/Checkpoint">000C90</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000C90</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Protective and Pathologic Roles of the Immune Response to Mouse Hepatitis Virus Type 1: Implications for Severe Acute Respiratory Syndrome<xref ref-type="fn" rid="fn3">▿</xref> </title><author><name sortKey="Khanolkar, Aaruni" sort="Khanolkar, Aaruni" uniqKey="Khanolkar A" first="Aaruni" last="Khanolkar">Aaruni Khanolkar</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Hartwig, Stacey M" sort="Hartwig, Stacey M" uniqKey="Hartwig S" first="Stacey M." last="Hartwig">Stacey M. Hartwig</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Haag, Brayton A" sort="Haag, Brayton A" uniqKey="Haag B" first="Brayton A." last="Haag">Brayton A. Haag</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Meyerholz, David K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K." last="Meyerholz">David K. Meyerholz</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Epping, Lecia L" sort="Epping, Lecia L" uniqKey="Epping L" first="Lecia L." last="Epping">Lecia L. Epping</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Haring, Jodie S" sort="Haring, Jodie S" uniqKey="Haring J" first="Jodie S." last="Haring">Jodie S. Haring</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Varga, Steven M" sort="Varga, Steven M" uniqKey="Varga S" first="Steven M." last="Varga">Steven M. Varga</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Harty, John T" sort="Harty, John T" uniqKey="Harty J" first="John T." last="Harty">John T. Harty</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Virology</title><idno type="ISSN">0022-538X</idno><idno type="eISSN">1098-5514</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>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.</p></div></front></TEI></pmc><pubmed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Protective and pathologic roles of the immune response to mouse hepatitis virus type 1: implications for severe acute respiratory syndrome.</title><author><name sortKey="Khanolkar, Aaruni" sort="Khanolkar, Aaruni" uniqKey="Khanolkar A" first="Aaruni" last="Khanolkar">Aaruni Khanolkar</name><affiliation wicri:level="4"><nlm:affiliation>Department of Microbiology, University of Iowa, Iowa City, 52242, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, University of Iowa, Iowa City, 52242</wicri:regionArea><orgName type="university">Université de l'Iowa</orgName><placeName><settlement type="city">Iowa City</settlement><region type="state">Iowa</region></placeName></affiliation></author><author><name sortKey="Hartwig, Stacey M" sort="Hartwig, Stacey M" uniqKey="Hartwig S" first="Stacey M" last="Hartwig">Stacey M. Hartwig</name></author><author><name sortKey="Haag, Brayton A" sort="Haag, Brayton A" uniqKey="Haag B" first="Brayton A" last="Haag">Brayton A. Haag</name></author><author><name sortKey="Meyerholz, David K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K" last="Meyerholz">David K. Meyerholz</name></author><author><name sortKey="Epping, Lecia L" sort="Epping, Lecia L" uniqKey="Epping L" first="Lecia L" last="Epping">Lecia L. Epping</name></author><author><name sortKey="Haring, Jodie S" sort="Haring, Jodie S" uniqKey="Haring J" first="Jodie S" last="Haring">Jodie S. Haring</name></author><author><name sortKey="Varga, Steven M" sort="Varga, Steven M" uniqKey="Varga S" first="Steven M" last="Varga">Steven M. Varga</name></author><author><name sortKey="Harty, John T" sort="Harty, John T" uniqKey="Harty J" first="John T" last="Harty">John T. Harty</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19570864</idno><idno type="pmid">19570864</idno><idno type="doi">10.1128/JVI.00355-09</idno><idno type="wicri:Area/PubMed/Corpus">001869</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001869</idno><idno type="wicri:Area/PubMed/Curation">001869</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001869</idno><idno type="wicri:Area/PubMed/Checkpoint">001812</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001812</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Protective and pathologic roles of the immune response to mouse hepatitis virus type 1: implications for severe acute respiratory syndrome.</title><author><name sortKey="Khanolkar, Aaruni" sort="Khanolkar, Aaruni" uniqKey="Khanolkar A" first="Aaruni" last="Khanolkar">Aaruni Khanolkar</name><affiliation wicri:level="4"><nlm:affiliation>Department of Microbiology, University of Iowa, Iowa City, 52242, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, University of Iowa, Iowa City, 52242</wicri:regionArea><orgName type="university">Université de l'Iowa</orgName><placeName><settlement type="city">Iowa City</settlement><region type="state">Iowa</region></placeName></affiliation></author><author><name sortKey="Hartwig, Stacey M" sort="Hartwig, Stacey M" uniqKey="Hartwig S" first="Stacey M" last="Hartwig">Stacey M. Hartwig</name></author><author><name sortKey="Haag, Brayton A" sort="Haag, Brayton A" uniqKey="Haag B" first="Brayton A" last="Haag">Brayton A. Haag</name></author><author><name sortKey="Meyerholz, David K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K" last="Meyerholz">David K. Meyerholz</name></author><author><name sortKey="Epping, Lecia L" sort="Epping, Lecia L" uniqKey="Epping L" first="Lecia L" last="Epping">Lecia L. Epping</name></author><author><name sortKey="Haring, Jodie S" sort="Haring, Jodie S" uniqKey="Haring J" first="Jodie S" last="Haring">Jodie S. Haring</name></author><author><name sortKey="Varga, Steven M" sort="Varga, Steven M" uniqKey="Varga S" first="Steven M" last="Varga">Steven M. Varga</name></author><author><name sortKey="Harty, John T" sort="Harty, John T" uniqKey="Harty J" first="John T" last="Harty">John T. Harty</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>CD4-Positive T-Lymphocytes (virology)</term><term>CD8-Positive T-Lymphocytes (virology)</term><term>Immune System (virology)</term><term>Immunity</term><term>Interferon Type I</term><term>Killer Cells, Natural (immunology)</term><term>Killer Cells, Natural (virology)</term><term>Mice</term><term>Mice, Inbred Strains</term><term>Murine hepatitis virus (immunology)</term><term>Murine hepatitis virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (etiology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Species Specificity</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules tueuses naturelles (immunologie)</term><term>Cellules tueuses naturelles (virologie)</term><term>Immunité</term><term>Interféron de type I</term><term>Lignées consanguines de souris</term><term>Lymphocytes T CD4+ (virologie)</term><term>Lymphocytes T CD8+ (virologie)</term><term>Réplication virale</term><term>Souris</term><term>Spécificité d'espèce</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (étiologie)</term><term>Système immunitaire (virologie)</term><term>Virus de l'hépatite murine (immunologie)</term><term>Virus de l'hépatite murine (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules tueuses naturelles</term><term>Syndrome respiratoire aigu sévère</term><term>Virus de l'hépatite murine</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Killer Cells, Natural</term><term>Murine hepatitis virus</term><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="MESH" 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>Spécificité d'espèce</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></pubmed></double></record>Pour manipuler ce document sous Unix (Dilib)
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