Differential virological and immunological outcome of severe acute respiratory syndrome coronavirus infection in susceptible and resistant transgenic mice expressing human angiotensin-converting enzyme 2.
Identifieur interne : 001941 ( PubMed/Corpus ); précédent : 001940; suivant : 001942Differential virological and immunological outcome of severe acute respiratory syndrome coronavirus infection in susceptible and resistant transgenic mice expressing human angiotensin-converting enzyme 2.
Auteurs : Naoko Yoshikawa ; Tomoki Yoshikawa ; Terence Hill ; Cheng Huang ; Douglas M. Watts ; Shinji Makino ; Gregg Milligan ; Tehsheng Chan ; Clarence J. Peters ; Chien-Te K. TsengSource :
- Journal of virology [ 1098-5514 ] ; 2009.
English descriptors
- KwdEn :
- Animals, Brain Diseases (virology), Cell Proliferation (drug effects), Concanavalin A (pharmacology), Cytokines (immunology), Gene Expression Regulation, Enzymologic, Genetic Predisposition to Disease (genetics), Humans, Kinetics, Lung Diseases (virology), Lymphocytes (cytology), Lymphocytes (drug effects), Lymphocytes (immunology), Mice, Mice, Transgenic, Organ Specificity, Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (metabolism), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Spleen (cytology), Spleen (drug effects), Spleen (immunology), Virus Replication.
- MESH :
- chemical , genetics : Peptidyl-Dipeptidase A.
- chemical , immunology : Cytokines.
- chemical , metabolism : Peptidyl-Dipeptidase A.
- chemical , pharmacology : Concanavalin A.
- cytology : Lymphocytes, Spleen.
- drug effects : Cell Proliferation, Lymphocytes, Spleen.
- genetics : Genetic Predisposition to Disease.
- immunology : Lymphocytes, SARS Virus, Severe Acute Respiratory Syndrome, Spleen.
- metabolism : Severe Acute Respiratory Syndrome.
- pathology : Severe Acute Respiratory Syndrome.
- virology : Brain Diseases, Lung Diseases, Severe Acute Respiratory Syndrome.
- Animals, Gene Expression Regulation, Enzymologic, Humans, Kinetics, Mice, Mice, Transgenic, Organ Specificity, Virus Replication.
Abstract
We previously reported that transgenic (Tg) mice expressing human angiotensin-converting enzyme 2 (hACE2), the receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), were highly susceptible to SARS-CoV infection, which resulted in the development of disease of various severity and even death in some lineages. In this study, we further characterized and compared the pathogeneses of SARS-CoV infection in two of the most stable Tg lineages, AC70 and AC22, representing those susceptible and resistant to the lethal SARS-CoV infection, respectively. The kinetics of virus replication and the inflammatory responses within the lungs and brains, as well as the clinical and pathological outcomes, were assessed in each lineage. In addition, we generated information on lymphocyte subsets and mitogen-mediated proliferation of splenocytes. We found that while both lineages were permissive to SARS-CoV infection, causing elevated secretion of many inflammatory mediators within the lungs and brains, viral infection appeared to be more intense in AC70 than in AC22 mice, especially in the brain. Moreover, such infection was accompanied by a more profound immune suppression in the former, as evidenced by the extensive loss of T cells, compromised responses to concanavalin A stimulation, and absence of inflammatory infiltrates within the brain. We also found that CD8(+) T cells were partially effective in attenuating the pathogenesis of SARS-CoV infection in lethality-resistant AC22 mice. Collectively, our data revealed a more intense viral infection and immunosuppression in AC70 mice than in AC22 mice, thereby providing us with an immunopathogenic basis for the fatal outcome of SARS-CoV infection in the AC70 mice.
DOI: 10.1128/JVI.02272-08
PubMed: 19297479
Links to Exploration step
pubmed:19297479Le document en format XML
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Watts</name></author><author><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name></author><author><name sortKey="Milligan, Gregg" sort="Milligan, Gregg" uniqKey="Milligan G" first="Gregg" last="Milligan">Gregg Milligan</name></author><author><name sortKey="Chan, Tehsheng" sort="Chan, Tehsheng" uniqKey="Chan T" first="Tehsheng" last="Chan">Tehsheng Chan</name></author><author><name sortKey="Peters, Clarence J" sort="Peters, Clarence J" uniqKey="Peters C" first="Clarence J" last="Peters">Clarence J. Peters</name></author><author><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K" last="Tseng">Chien-Te K. Tseng</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19297479</idno><idno type="pmid">19297479</idno><idno type="doi">10.1128/JVI.02272-08</idno><idno type="wicri:Area/PubMed/Corpus">001941</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001941</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Differential virological and immunological outcome of severe acute respiratory syndrome coronavirus infection in susceptible and resistant transgenic mice expressing human angiotensin-converting enzyme 2.</title><author><name sortKey="Yoshikawa, Naoko" sort="Yoshikawa, Naoko" uniqKey="Yoshikawa N" first="Naoko" last="Yoshikawa">Naoko Yoshikawa</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-0609, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Yoshikawa, Tomoki" sort="Yoshikawa, Tomoki" uniqKey="Yoshikawa T" first="Tomoki" last="Yoshikawa">Tomoki Yoshikawa</name></author><author><name sortKey="Hill, Terence" sort="Hill, Terence" uniqKey="Hill T" first="Terence" last="Hill">Terence Hill</name></author><author><name sortKey="Huang, Cheng" sort="Huang, Cheng" uniqKey="Huang C" first="Cheng" last="Huang">Cheng Huang</name></author><author><name sortKey="Watts, Douglas M" sort="Watts, Douglas M" uniqKey="Watts D" first="Douglas M" last="Watts">Douglas M. Watts</name></author><author><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name></author><author><name sortKey="Milligan, Gregg" sort="Milligan, Gregg" uniqKey="Milligan G" first="Gregg" last="Milligan">Gregg Milligan</name></author><author><name sortKey="Chan, Tehsheng" sort="Chan, Tehsheng" uniqKey="Chan T" first="Tehsheng" last="Chan">Tehsheng Chan</name></author><author><name sortKey="Peters, Clarence J" sort="Peters, Clarence J" uniqKey="Peters C" first="Clarence J" last="Peters">Clarence J. Peters</name></author><author><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K" last="Tseng">Chien-Te K. Tseng</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>Brain Diseases (virology)</term><term>Cell Proliferation (drug effects)</term><term>Concanavalin A (pharmacology)</term><term>Cytokines (immunology)</term><term>Gene Expression Regulation, Enzymologic</term><term>Genetic Predisposition to Disease (genetics)</term><term>Humans</term><term>Kinetics</term><term>Lung Diseases (virology)</term><term>Lymphocytes (cytology)</term><term>Lymphocytes (drug effects)</term><term>Lymphocytes (immunology)</term><term>Mice</term><term>Mice, Transgenic</term><term>Organ Specificity</term><term>Peptidyl-Dipeptidase A (genetics)</term><term>Peptidyl-Dipeptidase A (metabolism)</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (metabolism)</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Spleen (cytology)</term><term>Spleen (drug effects)</term><term>Spleen (immunology)</term><term>Virus Replication</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Concanavalin A</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Lymphocytes</term><term>Spleen</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Proliferation</term><term>Lymphocytes</term><term>Spleen</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Genetic Predisposition to Disease</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lymphocytes</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term><term>Spleen</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Brain Diseases</term><term>Lung Diseases</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Expression Regulation, Enzymologic</term><term>Humans</term><term>Kinetics</term><term>Mice</term><term>Mice, Transgenic</term><term>Organ Specificity</term><term>Virus Replication</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We previously reported that transgenic (Tg) mice expressing human angiotensin-converting enzyme 2 (hACE2), the receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), were highly susceptible to SARS-CoV infection, which resulted in the development of disease of various severity and even death in some lineages. In this study, we further characterized and compared the pathogeneses of SARS-CoV infection in two of the most stable Tg lineages, AC70 and AC22, representing those susceptible and resistant to the lethal SARS-CoV infection, respectively. The kinetics of virus replication and the inflammatory responses within the lungs and brains, as well as the clinical and pathological outcomes, were assessed in each lineage. In addition, we generated information on lymphocyte subsets and mitogen-mediated proliferation of splenocytes. We found that while both lineages were permissive to SARS-CoV infection, causing elevated secretion of many inflammatory mediators within the lungs and brains, viral infection appeared to be more intense in AC70 than in AC22 mice, especially in the brain. Moreover, such infection was accompanied by a more profound immune suppression in the former, as evidenced by the extensive loss of T cells, compromised responses to concanavalin A stimulation, and absence of inflammatory infiltrates within the brain. We also found that CD8(+) T cells were partially effective in attenuating the pathogenesis of SARS-CoV infection in lethality-resistant AC22 mice. Collectively, our data revealed a more intense viral infection and immunosuppression in AC70 mice than in AC22 mice, thereby providing us with an immunopathogenic basis for the fatal outcome of SARS-CoV infection in the AC70 mice.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19297479</PMID><DateCompleted><Year>2009</Year><Month>05</Month><Day>29</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>83</Volume><Issue>11</Issue><PubDate><Year>2009</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Differential virological and immunological outcome of severe acute respiratory syndrome coronavirus infection in susceptible and resistant transgenic mice expressing human angiotensin-converting enzyme 2.</ArticleTitle><Pagination><MedlinePgn>5451-65</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.02272-08</ELocationID><Abstract><AbstractText>We previously reported that transgenic (Tg) mice expressing human angiotensin-converting enzyme 2 (hACE2), the receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), were highly susceptible to SARS-CoV infection, which resulted in the development of disease of various severity and even death in some lineages. In this study, we further characterized and compared the pathogeneses of SARS-CoV infection in two of the most stable Tg lineages, AC70 and AC22, representing those susceptible and resistant to the lethal SARS-CoV infection, respectively. The kinetics of virus replication and the inflammatory responses within the lungs and brains, as well as the clinical and pathological outcomes, were assessed in each lineage. In addition, we generated information on lymphocyte subsets and mitogen-mediated proliferation of splenocytes. We found that while both lineages were permissive to SARS-CoV infection, causing elevated secretion of many inflammatory mediators within the lungs and brains, viral infection appeared to be more intense in AC70 than in AC22 mice, especially in the brain. Moreover, such infection was accompanied by a more profound immune suppression in the former, as evidenced by the extensive loss of T cells, compromised responses to concanavalin A stimulation, and absence of inflammatory infiltrates within the brain. We also found that CD8(+) T cells were partially effective in attenuating the pathogenesis of SARS-CoV infection in lethality-resistant AC22 mice. Collectively, our data revealed a more intense viral infection and immunosuppression in AC70 mice than in AC22 mice, thereby providing us with an immunopathogenic basis for the fatal outcome of SARS-CoV infection in the AC70 mice.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yoshikawa</LastName><ForeName>Naoko</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-0609, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yoshikawa</LastName><ForeName>Tomoki</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Hill</LastName><ForeName>Terence</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Cheng</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Watts</LastName><ForeName>Douglas M</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Makino</LastName><ForeName>Shinji</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Milligan</LastName><ForeName>Gregg</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Tehsheng</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Peters</LastName><ForeName>Clarence J</ForeName><Initials>CJ</Initials></Author><Author ValidYN="Y"><LastName>Tseng</LastName><ForeName>Chien-Te K</ForeName><Initials>CT</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01AI30039</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 AI057156</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI063118</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01AI25489</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21AI072201</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21AI063118</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI072201</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01 AI30039</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>03</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>11028-71-0</RegistryNumber><NameOfSubstance UI="D003208">Concanavalin A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.15.1</RegistryNumber><NameOfSubstance UI="D007703">Peptidyl-Dipeptidase A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.17.-</RegistryNumber><NameOfSubstance UI="C413524">angiotensin converting enzyme 2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001927" MajorTopicYN="N">Brain Diseases</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003208" MajorTopicYN="N">Concanavalin A</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015971" MajorTopicYN="N">Gene Expression Regulation, Enzymologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="Y">Genetic Predisposition to Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008171" MajorTopicYN="N">Lung Diseases</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008214" MajorTopicYN="N">Lymphocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009928" MajorTopicYN="N">Organ Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013154" MajorTopicYN="N">Spleen</DescriptorName><QualifierName UI="Q000166" 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