Effects of Toll-like receptor stimulation on eosinophilic infiltration in lungs of BALB/c mice immunized with UV-inactivated severe acute respiratory syndrome-related coronavirus vaccine.
Identifieur interne : 001005 ( PubMed/Checkpoint ); précédent : 001004; suivant : 001006Effects of Toll-like receptor stimulation on eosinophilic infiltration in lungs of BALB/c mice immunized with UV-inactivated severe acute respiratory syndrome-related coronavirus vaccine.
Auteurs : Naoko Iwata-Yoshikawa [Japon] ; Akihiko Uda [Japon] ; Tadaki Suzuki [Japon] ; Yasuko Tsunetsugu-Yokota [Japon] ; Yuko Sato [Japon] ; Shigeru Morikawa [Japon] ; Masato Tashiro [Japon] ; Tetsutaro Sata [Japon] ; Hideki Hasegawa [Japon] ; Noriyo Nagata [Japon]Source :
- Journal of virology [ 1098-5514 ] ; 2014.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes, Analyse de survie, Analyse sur microréseau, Animaux, Chimiokines (analyse), Granulocytes éosinophiles (immunologie), Interleukine-13 (analyse), Interleukine-4 (analyse), Poumon (anatomopathologie), Poumon (immunologie), Récepteurs de type Toll (agonistes), Récepteurs de type Toll (immunologie), Récepteurs viraux, Souris, Souris de lignée BALB C, Syndrome respiratoire aigu sévère (immunologie), Vaccins antiviraux (administration et posologie), Vaccins antiviraux (immunologie), Vaccins inactivés (administration et posologie), Vaccins inactivés (immunologie), Virus du SRAS (immunologie).
- MESH :
- administration et posologie : Vaccins antiviraux, Vaccins inactivés.
- agonistes : Récepteurs de type Toll.
- analyse : Chimiokines, Interleukine-13, Interleukine-4.
- anatomopathologie : Poumon.
- immunologie : Granulocytes éosinophiles, Poumon, Récepteurs de type Toll, Syndrome respiratoire aigu sévère, Vaccins antiviraux, Vaccins inactivés, Virus du SRAS.
- Analyse de profil d'expression de gènes, Analyse de survie, Analyse sur microréseau, Animaux, Récepteurs viraux, Souris, Souris de lignée BALB C.
English descriptors
- KwdEn :
- Animals, Chemokines (analysis), Eosinophils (immunology), Gene Expression Profiling, Interleukin-13 (analysis), Interleukin-4 (analysis), Lung (immunology), Lung (pathology), Mice, Mice, Inbred BALB C, Microarray Analysis, Receptors, Virus, SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Survival Analysis, Toll-Like Receptors (agonists), Toll-Like Receptors (immunology), Vaccines, Inactivated (administration & dosage), Vaccines, Inactivated (immunology), Viral Vaccines (administration & dosage), Viral Vaccines (immunology).
- MESH :
- chemical , administration & dosage : Vaccines, Inactivated, Viral Vaccines.
- chemical , agonists : Toll-Like Receptors.
- chemical , analysis : Chemokines, Interleukin-13, Interleukin-4.
- immunology : Eosinophils, Lung, SARS Virus, Severe Acute Respiratory Syndrome, Toll-Like Receptors, Vaccines, Inactivated, Viral Vaccines.
- pathology : Lung.
- Animals, Gene Expression Profiling, Mice, Mice, Inbred BALB C, Microarray Analysis, Receptors, Virus, Survival Analysis.
Abstract
Severe acute respiratory syndrome-related coronavirus (SARS-CoV) is an emerging pathogen that causes severe respiratory illness. Whole UV-inactivated SARS-CoV (UV-V), bearing multiple epitopes and proteins, is a candidate vaccine against this virus. However, whole inactivated SARS vaccine that includes nucleocapsid protein is reported to induce eosinophilic infiltration in mouse lungs after challenge with live SARS-CoV. In this study, an ability of Toll-like receptor (TLR) agonists to reduce the side effects of UV-V vaccination in a 6-month-old adult BALB/c mouse model was investigated, using the mouse-passaged Frankfurt 1 isolate of SARS-CoV. Immunization of adult mice with UV-V, with or without alum, resulted in partial protection from lethal doses of SARS-CoV challenge, but extensive eosinophil infiltration in the lungs was observed. In contrast, TLR agonists added to UV-V vaccine, including lipopolysaccharide, poly(U), and poly(I·C) (UV-V+TLR), strikingly reduced excess eosinophilic infiltration in the lungs and induced lower levels of interleukin-4 and -13 and eotaxin in the lungs than UV-V-immunization alone. Additionally, microarray analysis showed that genes associated with chemotaxis, eosinophil migration, eosinophilia, and cell movement and the polarization of Th2 cells were upregulated in UV-V-immunized but not in UV-V+TLR-immunized mice. In particular, CD11b(+) cells in the lungs of UV-V-immunized mice showed the upregulation of genes associated with the induction of eosinophils after challenge. These findings suggest that vaccine-induced eosinophil immunopathology in the lungs upon SARS-CoV infection could be avoided by the TLR agonist adjuvants.
DOI: 10.1128/JVI.00983-14
PubMed: 24850731
Affiliations:
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uniqKey="Hasegawa H" first="Hideki" last="Hasegawa">Hideki Hasegawa</name><affiliation wicri:level="3"><nlm:affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Nagata, Noriyo" sort="Nagata, Noriyo" uniqKey="Nagata N" first="Noriyo" last="Nagata">Noriyo Nagata</name><affiliation wicri:level="3"><nlm:affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan nnagata@niid.go.jp.</nlm:affiliation><country wicri:rule="url">Japon</country><wicri:regionArea>Department of Pathology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement 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syndrome-related coronavirus vaccine.</title><author><name sortKey="Iwata Yoshikawa, Naoko" sort="Iwata Yoshikawa, Naoko" uniqKey="Iwata Yoshikawa N" first="Naoko" last="Iwata-Yoshikawa">Naoko Iwata-Yoshikawa</name><affiliation wicri:level="3"><nlm:affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Uda, Akihiko" sort="Uda, Akihiko" uniqKey="Uda A" first="Akihiko" last="Uda">Akihiko Uda</name><affiliation wicri:level="3"><nlm:affiliation>Department of Veterinary Science, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Veterinary Science, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Suzuki, Tadaki" sort="Suzuki, Tadaki" uniqKey="Suzuki T" first="Tadaki" last="Suzuki">Tadaki Suzuki</name><affiliation wicri:level="3"><nlm:affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Tsunetsugu Yokota, Yasuko" sort="Tsunetsugu Yokota, Yasuko" uniqKey="Tsunetsugu Yokota Y" first="Yasuko" last="Tsunetsugu-Yokota">Yasuko Tsunetsugu-Yokota</name><affiliation wicri:level="3"><nlm:affiliation>Department of Immunology, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Immunology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Sato, Yuko" sort="Sato, Yuko" uniqKey="Sato Y" first="Yuko" last="Sato">Yuko Sato</name><affiliation wicri:level="3"><nlm:affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Morikawa, Shigeru" sort="Morikawa, Shigeru" uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name><affiliation wicri:level="3"><nlm:affiliation>Department of Veterinary Science, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Veterinary Science, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Tashiro, Masato" sort="Tashiro, Masato" uniqKey="Tashiro M" first="Masato" last="Tashiro">Masato Tashiro</name><affiliation wicri:level="3"><nlm:affiliation>Influenza Virus Research Center, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Influenza Virus Research Center, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Sata, Tetsutaro" sort="Sata, Tetsutaro" uniqKey="Sata T" first="Tetsutaro" last="Sata">Tetsutaro Sata</name><affiliation wicri:level="3"><nlm:affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Hasegawa, Hideki" sort="Hasegawa, Hideki" uniqKey="Hasegawa H" first="Hideki" last="Hasegawa">Hideki Hasegawa</name><affiliation wicri:level="3"><nlm:affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Nagata, Noriyo" sort="Nagata, Noriyo" uniqKey="Nagata N" first="Noriyo" last="Nagata">Noriyo Nagata</name><affiliation wicri:level="3"><nlm:affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan nnagata@niid.go.jp.</nlm:affiliation><country wicri:rule="url">Japon</country><wicri:regionArea>Department of Pathology, National Institute of Infectious Diseases, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Chemokines (analysis)</term><term>Eosinophils (immunology)</term><term>Gene Expression Profiling</term><term>Interleukin-13 (analysis)</term><term>Interleukin-4 (analysis)</term><term>Lung (immunology)</term><term>Lung (pathology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Microarray Analysis</term><term>Receptors, Virus</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Survival Analysis</term><term>Toll-Like Receptors (agonists)</term><term>Toll-Like Receptors (immunology)</term><term>Vaccines, Inactivated (administration & dosage)</term><term>Vaccines, Inactivated (immunology)</term><term>Viral Vaccines (administration & dosage)</term><term>Viral Vaccines (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Analyse de survie</term><term>Analyse sur microréseau</term><term>Animaux</term><term>Chimiokines (analyse)</term><term>Granulocytes éosinophiles (immunologie)</term><term>Interleukine-13 (analyse)</term><term>Interleukine-4 (analyse)</term><term>Poumon (anatomopathologie)</term><term>Poumon (immunologie)</term><term>Récepteurs de type Toll (agonistes)</term><term>Récepteurs de type Toll (immunologie)</term><term>Récepteurs viraux</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Vaccins antiviraux (administration et posologie)</term><term>Vaccins antiviraux (immunologie)</term><term>Vaccins inactivés (administration et posologie)</term><term>Vaccins inactivés (immunologie)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Vaccines, Inactivated</term><term>Viral Vaccines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Toll-Like Receptors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Chemokines</term><term>Interleukin-13</term><term>Interleukin-4</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Vaccins antiviraux</term><term>Vaccins inactivés</term></keywords><keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Récepteurs de type Toll</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Chimiokines</term><term>Interleukine-13</term><term>Interleukine-4</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Granulocytes éosinophiles</term><term>Poumon</term><term>Récepteurs de type Toll</term><term>Syndrome respiratoire aigu sévère</term><term>Vaccins antiviraux</term><term>Vaccins inactivés</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Eosinophils</term><term>Lung</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term><term>Toll-Like Receptors</term><term>Vaccines, Inactivated</term><term>Viral Vaccines</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Expression Profiling</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Microarray Analysis</term><term>Receptors, Virus</term><term>Survival Analysis</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Analyse de survie</term><term>Analyse sur microréseau</term><term>Animaux</term><term>Récepteurs viraux</term><term>Souris</term><term>Souris de lignée BALB C</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome-related coronavirus (SARS-CoV) is an emerging pathogen that causes severe respiratory illness. Whole UV-inactivated SARS-CoV (UV-V), bearing multiple epitopes and proteins, is a candidate vaccine against this virus. However, whole inactivated SARS vaccine that includes nucleocapsid protein is reported to induce eosinophilic infiltration in mouse lungs after challenge with live SARS-CoV. In this study, an ability of Toll-like receptor (TLR) agonists to reduce the side effects of UV-V vaccination in a 6-month-old adult BALB/c mouse model was investigated, using the mouse-passaged Frankfurt 1 isolate of SARS-CoV. Immunization of adult mice with UV-V, with or without alum, resulted in partial protection from lethal doses of SARS-CoV challenge, but extensive eosinophil infiltration in the lungs was observed. In contrast, TLR agonists added to UV-V vaccine, including lipopolysaccharide, poly(U), and poly(I·C) (UV-V+TLR), strikingly reduced excess eosinophilic infiltration in the lungs and induced lower levels of interleukin-4 and -13 and eotaxin in the lungs than UV-V-immunization alone. Additionally, microarray analysis showed that genes associated with chemotaxis, eosinophil migration, eosinophilia, and cell movement and the polarization of Th2 cells were upregulated in UV-V-immunized but not in UV-V+TLR-immunized mice. In particular, CD11b(+) cells in the lungs of UV-V-immunized mice showed the upregulation of genes associated with the induction of eosinophils after challenge. These findings suggest that vaccine-induced eosinophil immunopathology in the lungs upon SARS-CoV infection could be avoided by the TLR agonist adjuvants.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24850731</PMID><DateCompleted><Year>2014</Year><Month>10</Month><Day>01</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>88</Volume><Issue>15</Issue><PubDate><Year>2014</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Effects of Toll-like receptor stimulation on eosinophilic infiltration in lungs of BALB/c mice immunized with UV-inactivated severe acute respiratory syndrome-related coronavirus vaccine.</ArticleTitle><Pagination><MedlinePgn>8597-614</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.00983-14</ELocationID><Abstract><AbstractText Label="UNLABELLED">Severe acute respiratory syndrome-related coronavirus (SARS-CoV) is an emerging pathogen that causes severe respiratory illness. Whole UV-inactivated SARS-CoV (UV-V), bearing multiple epitopes and proteins, is a candidate vaccine against this virus. However, whole inactivated SARS vaccine that includes nucleocapsid protein is reported to induce eosinophilic infiltration in mouse lungs after challenge with live SARS-CoV. In this study, an ability of Toll-like receptor (TLR) agonists to reduce the side effects of UV-V vaccination in a 6-month-old adult BALB/c mouse model was investigated, using the mouse-passaged Frankfurt 1 isolate of SARS-CoV. Immunization of adult mice with UV-V, with or without alum, resulted in partial protection from lethal doses of SARS-CoV challenge, but extensive eosinophil infiltration in the lungs was observed. In contrast, TLR agonists added to UV-V vaccine, including lipopolysaccharide, poly(U), and poly(I·C) (UV-V+TLR), strikingly reduced excess eosinophilic infiltration in the lungs and induced lower levels of interleukin-4 and -13 and eotaxin in the lungs than UV-V-immunization alone. Additionally, microarray analysis showed that genes associated with chemotaxis, eosinophil migration, eosinophilia, and cell movement and the polarization of Th2 cells were upregulated in UV-V-immunized but not in UV-V+TLR-immunized mice. In particular, CD11b(+) cells in the lungs of UV-V-immunized mice showed the upregulation of genes associated with the induction of eosinophils after challenge. These findings suggest that vaccine-induced eosinophil immunopathology in the lungs upon SARS-CoV infection could be avoided by the TLR agonist adjuvants.</AbstractText><AbstractText Label="IMPORTANCE" NlmCategory="OBJECTIVE">Inactivated whole severe acute respiratory syndrome-related coronavirus (SARS-CoV) vaccines induce neutralizing antibodies in mouse models; however, they also cause increased eosinophilic immunopathology in the lungs upon SARS-CoV challenge. In this study, the ability of adjuvant Toll-like receptor (TLR) agonists to reduce the side effects of UV-inactivated SARS-CoV vaccination in a BALB/c mouse model was tested, using the mouse-passaged Frankfurt 1 isolate of SARS-CoV. We found that TLR stimulation reduced the high level of eosinophilic infiltration that occurred in the lungs of mice immunized with UV-inactivated SARS-CoV. Microarray analysis revealed that genes associated with chemotaxis, eosinophil migration, eosinophilia, and cell movement and the polarization of Th2 cells were upregulated in UV-inactivated SARS-CoV-immunized mice. This study may be helpful for elucidating the pathogenesis underlying eosinophilic infiltration resulting from immunization with inactivated vaccine.</AbstractText><CopyrightInformation>Copyright © 2014, American Society for Microbiology. All Rights Reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Iwata-Yoshikawa</LastName><ForeName>Naoko</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Uda</LastName><ForeName>Akihiko</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Veterinary Science, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suzuki</LastName><ForeName>Tadaki</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsunetsugu-Yokota</LastName><ForeName>Yasuko</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Immunology, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sato</LastName><ForeName>Yuko</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morikawa</LastName><ForeName>Shigeru</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Veterinary Science, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tashiro</LastName><ForeName>Masato</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Influenza Virus Research Center, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sata</LastName><ForeName>Tetsutaro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hasegawa</LastName><ForeName>Hideki</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagata</LastName><ForeName>Noriyo</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan nnagata@niid.go.jp.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>05</Month><Day>21</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="D018925">Chemokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018793">Interleukin-13</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011991">Receptors, Virus</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051193">Toll-Like Receptors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015164">Vaccines, Inactivated</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014765">Viral Vaccines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C078034">coronavirus receptors</NameOfSubstance></Chemical><Chemical><RegistryNumber>207137-56-2</RegistryNumber><NameOfSubstance UI="D015847">Interleukin-4</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018925" MajorTopicYN="N">Chemokines</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004804" MajorTopicYN="N">Eosinophils</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018793" MajorTopicYN="N">Interleukin-13</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015847" MajorTopicYN="N">Interleukin-4</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D046228" MajorTopicYN="N">Microarray Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011991" MajorTopicYN="N">Receptors, Virus</DescriptorName></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></MeshHeading><MeshHeading><DescriptorName UI="D016019" MajorTopicYN="N">Survival Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051193" MajorTopicYN="N">Toll-Like Receptors</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="Y">agonists</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015164" MajorTopicYN="N">Vaccines, Inactivated</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014765" 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