Cellular immune responses to severe acute respiratory syndrome coronavirus (SARS-CoV) infection in senescent BALB/c mice: CD4+ T cells are important in control of SARS-CoV infection.
Identifieur interne : 001795 ( PubMed/Corpus ); précédent : 001794; suivant : 001796Cellular immune responses to severe acute respiratory syndrome coronavirus (SARS-CoV) infection in senescent BALB/c mice: CD4+ T cells are important in control of SARS-CoV infection.
Auteurs : Jun Chen ; Yuk Fai Lau ; Elaine W. Lamirande ; Christopher D. Paddock ; Jeanine H. Bartlett ; Sherif R. Zaki ; Kanta SubbaraoSource :
- Journal of virology [ 1098-5514 ] ; 2010.
English descriptors
- KwdEn :
- Animals, Base Sequence, CD4-Positive T-Lymphocytes (immunology), DNA Primers, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Inflammation Mediators (physiology), Mice, Mice, Inbred BALB C, Pneumonia (complications), Pneumonia (pathology), Polymerase Chain Reaction, SARS Virus (physiology), Severe Acute Respiratory Syndrome (complications), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology).
- MESH :
- chemical , physiology : Inflammation Mediators.
- chemical : DNA Primers.
- complications : Pneumonia, Severe Acute Respiratory Syndrome.
- immunology : CD4-Positive T-Lymphocytes, Severe Acute Respiratory Syndrome.
- pathology : Pneumonia, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- Animals, Base Sequence, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Mice, Mice, Inbred BALB C, Polymerase Chain Reaction.
Abstract
We characterized the cellular immune response to severe acute respiratory syndrome coronavirus (SARS-CoV) infection in 12- to 14-month-old BALB/c mice, a model that mimics features of the human disease. Following intranasal administration, the virus replicated in the lungs, with peak titers on day 2 postinfection. Enhanced production of cytokines (tumor necrosis factor alpha [TNF-alpha] and interleukin-6 [IL-6]) and chemokines (CXCL10, CCL2, CCL3, and CCL5) correlated with migration of NK cells, macrophages, and plasmacytoid dendritic cells (pDC) into the lungs. By day 7, histopathologic evidence of pneumonitis was seen in the lungs when viral clearance occurred. At this time, a second wave of enhanced production of cytokines (TNF-alpha, IL-6, gamma interferon [IFN-gamma], IL-2, and IL-5), chemokines (CXCL9, CXCL10, CCL2, CCL3, and CCL5), and receptors (CXCR3, CCR2, and CCR5), was detected in the lungs, associated with an influx of T lymphocytes. Depletion of CD8(+) T cells at the time of infection did not affect viral replication or clearance. However, depletion of CD4(+) T cells resulted in an enhanced immune-mediated interstitial pneumonitis and delayed clearance of SARS-CoV from the lungs, which was associated with reduced neutralizing antibody and cytokine production and reduced pulmonary recruitment of lymphocytes. Innate defense mechanisms are able to control SARS-CoV infection in the absence of CD4(+) and CD8(+) T cells and antibodies. Our findings provide new insights into the pathogenesis of SARS, demonstrating the important role of CD4(+) but not CD8(+) T cells in primary SARS-CoV infection in this model.
DOI: 10.1128/JVI.01281-09
PubMed: 19906920
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pubmed:19906920Le document en format XML
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Lamirande</name></author><author><name sortKey="Paddock, Christopher D" sort="Paddock, Christopher D" uniqKey="Paddock C" first="Christopher D" last="Paddock">Christopher D. Paddock</name></author><author><name sortKey="Bartlett, Jeanine H" sort="Bartlett, Jeanine H" uniqKey="Bartlett J" first="Jeanine H" last="Bartlett">Jeanine H. Bartlett</name></author><author><name sortKey="Zaki, Sherif R" sort="Zaki, Sherif R" uniqKey="Zaki S" first="Sherif R" last="Zaki">Sherif R. 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Zaki</name></author><author><name sortKey="Subbarao, Kanta" sort="Subbarao, Kanta" uniqKey="Subbarao K" first="Kanta" last="Subbarao">Kanta Subbarao</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>DNA Primers</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Flow Cytometry</term><term>Inflammation Mediators (physiology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Pneumonia (complications)</term><term>Pneumonia (pathology)</term><term>Polymerase Chain Reaction</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (complications)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Inflammation Mediators</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>DNA Primers</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Pneumonia</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Pneumonia</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Flow Cytometry</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Polymerase Chain Reaction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We characterized the cellular immune response to severe acute respiratory syndrome coronavirus (SARS-CoV) infection in 12- to 14-month-old BALB/c mice, a model that mimics features of the human disease. Following intranasal administration, the virus replicated in the lungs, with peak titers on day 2 postinfection. Enhanced production of cytokines (tumor necrosis factor alpha [TNF-alpha] and interleukin-6 [IL-6]) and chemokines (CXCL10, CCL2, CCL3, and CCL5) correlated with migration of NK cells, macrophages, and plasmacytoid dendritic cells (pDC) into the lungs. By day 7, histopathologic evidence of pneumonitis was seen in the lungs when viral clearance occurred. At this time, a second wave of enhanced production of cytokines (TNF-alpha, IL-6, gamma interferon [IFN-gamma], IL-2, and IL-5), chemokines (CXCL9, CXCL10, CCL2, CCL3, and CCL5), and receptors (CXCR3, CCR2, and CCR5), was detected in the lungs, associated with an influx of T lymphocytes. Depletion of CD8(+) T cells at the time of infection did not affect viral replication or clearance. However, depletion of CD4(+) T cells resulted in an enhanced immune-mediated interstitial pneumonitis and delayed clearance of SARS-CoV from the lungs, which was associated with reduced neutralizing antibody and cytokine production and reduced pulmonary recruitment of lymphocytes. Innate defense mechanisms are able to control SARS-CoV infection in the absence of CD4(+) and CD8(+) T cells and antibodies. Our findings provide new insights into the pathogenesis of SARS, demonstrating the important role of CD4(+) but not CD8(+) T cells in primary SARS-CoV infection in this model.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19906920</PMID><DateCompleted><Year>2010</Year><Month>02</Month><Day>18</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>84</Volume><Issue>3</Issue><PubDate><Year>2010</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Cellular immune responses to severe acute respiratory syndrome coronavirus (SARS-CoV) infection in senescent BALB/c mice: CD4+ T cells are important in control of SARS-CoV infection.</ArticleTitle><Pagination><MedlinePgn>1289-301</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.01281-09</ELocationID><Abstract><AbstractText>We characterized the cellular immune response to severe acute respiratory syndrome coronavirus (SARS-CoV) infection in 12- to 14-month-old BALB/c mice, a model that mimics features of the human disease. Following intranasal administration, the virus replicated in the lungs, with peak titers on day 2 postinfection. Enhanced production of cytokines (tumor necrosis factor alpha [TNF-alpha] and interleukin-6 [IL-6]) and chemokines (CXCL10, CCL2, CCL3, and CCL5) correlated with migration of NK cells, macrophages, and plasmacytoid dendritic cells (pDC) into the lungs. By day 7, histopathologic evidence of pneumonitis was seen in the lungs when viral clearance occurred. At this time, a second wave of enhanced production of cytokines (TNF-alpha, IL-6, gamma interferon [IFN-gamma], IL-2, and IL-5), chemokines (CXCL9, CXCL10, CCL2, CCL3, and CCL5), and receptors (CXCR3, CCR2, and CCR5), was detected in the lungs, associated with an influx of T lymphocytes. Depletion of CD8(+) T cells at the time of infection did not affect viral replication or clearance. However, depletion of CD4(+) T cells resulted in an enhanced immune-mediated interstitial pneumonitis and delayed clearance of SARS-CoV from the lungs, which was associated with reduced neutralizing antibody and cytokine production and reduced pulmonary recruitment of lymphocytes. Innate defense mechanisms are able to control SARS-CoV infection in the absence of CD4(+) and CD8(+) T cells and antibodies. Our findings provide new insights into the pathogenesis of SARS, demonstrating the important role of CD4(+) but not CD8(+) T cells in primary SARS-CoV infection in this model.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institute for Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892-3203, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lau</LastName><ForeName>Yuk Fai</ForeName><Initials>YF</Initials></Author><Author ValidYN="Y"><LastName>Lamirande</LastName><ForeName>Elaine W</ForeName><Initials>EW</Initials></Author><Author ValidYN="Y"><LastName>Paddock</LastName><ForeName>Christopher D</ForeName><Initials>CD</Initials></Author><Author ValidYN="Y"><LastName>Bartlett</LastName><ForeName>Jeanine H</ForeName><Initials>JH</Initials></Author><Author ValidYN="Y"><LastName>Zaki</LastName><ForeName>Sherif R</ForeName><Initials>SR</Initials></Author><Author ValidYN="Y"><LastName>Subbarao</LastName><ForeName>Kanta</ForeName><Initials>K</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>11</Month><Day>11</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="D017931">DNA 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