Experimental infection of macaques with the human reovirus BYD1 strain: an animal model for the study of the severe acute respiratory syndrome.
Identifieur interne : 002595 ( PubMed/Corpus ); précédent : 002594; suivant : 002596Experimental infection of macaques with the human reovirus BYD1 strain: an animal model for the study of the severe acute respiratory syndrome.
Auteurs : Cheng He ; Wanyong Pang ; Xinhao Yong ; Hong Zhu ; Ming Lei ; Qing DuanSource :
- DNA and cell biology [ 1044-5498 ] ; 2005.
English descriptors
- KwdEn :
- Animals, Antibodies, Viral (blood), Cell Line, Tumor, Chlorocebus aethiops, Disease Models, Animal, Female, Fever (pathology), Humans, Lung (pathology), Lymph Nodes (pathology), Macaca, Male, Pulmonary Alveoli (pathology), Reoviridae (immunology), Reoviridae (isolation & purification), Reoviridae (pathogenicity), Reoviridae Infections (immunology), Reoviridae Infections (pathology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Spleen (pathology), Vero Cells.
- MESH :
- chemical , blood : Antibodies, Viral.
- immunology : Reoviridae, Reoviridae Infections, Severe Acute Respiratory Syndrome.
- isolation & purification : Reoviridae.
- pathogenicity : Reoviridae.
- pathology : Fever, Lung, Lymph Nodes, Pulmonary Alveoli, Reoviridae Infections, Severe Acute Respiratory Syndrome, Spleen.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Tumor, Chlorocebus aethiops, Disease Models, Animal, Female, Humans, Macaca, Male, Vero Cells.
Abstract
Experimental studies were performed to determine the role of a newly isolated reovirus (ReoV) from a severe acute respiratory syndrome (SARS) patient in the etiology of this newly described serious respiratory syndrome. Four cynomologus macaques were inoculated with this reovirus (BYD1) in an attempt to replicate the infection and pathology observed in SARS. The body temperature of the infected monkeys was monitored three times a day, and blood and fecal samples were periodically collected for specific immunology determinations. On days 7 and 33 after inoculation, necropsies for pathological accessment and pathogen isolation were performed. The four infected macaques developed a fever on days 3 and 4 after inoculation, and maintainted a febrile state for 4-6 days. The highest temperature in the animals recorded was 40.4 degrees C. After a recovery phase, the macaques developed a second febrile condition. Antibody titers against the reovirus injected by the intravenous route occurred in higher number than those in the nasal cavity. Four macaque monkeys demonstrated diffuse alveolar damage, characterized by hemorrhagic pneumonia, serosanguineous exudates, formation of hyaline membranes, and type II pneumocyte hyperplasia, which were similar to those that have been noted in SARS patients. Lymphocytes decreased in the cortex of the lymph node and in the white pulp of the spleen. ReoV was detected in pneumonic tissue by virus isolation and RT-PCR. The macaques infected with the newly isolated reovirus developed a fever, diffuse alveolar damage and pulmonary interstitial inflammation similar to that noted in SARS patients. This evidence demonstrates that ReoV might have a primary role in the etiology of SARS.
DOI: 10.1089/dna.2005.24.491
PubMed: 16101346
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pubmed:16101346Le document en format XML
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last="Lei">Ming Lei</name></author><author><name sortKey="Duan, Qing" sort="Duan, Qing" uniqKey="Duan Q" first="Qing" last="Duan">Qing Duan</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:16101346</idno><idno type="pmid">16101346</idno><idno type="doi">10.1089/dna.2005.24.491</idno><idno type="wicri:Area/PubMed/Corpus">002595</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002595</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Experimental infection of macaques with the human reovirus BYD1 strain: an animal model for the study of the severe acute respiratory syndrome.</title><author><name sortKey="He, Cheng" sort="He, Cheng" uniqKey="He C" first="Cheng" last="He">Cheng He</name><affiliation><nlm:affiliation>Laboratory Animal Institute, College of Veterinary Medicine, China Agricultural University, Beijing, People's Republic of China. hecheng@cau.edu.cn</nlm:affiliation></affiliation></author><author><name sortKey="Pang, Wanyong" sort="Pang, Wanyong" uniqKey="Pang W" first="Wanyong" last="Pang">Wanyong Pang</name></author><author><name sortKey="Yong, Xinhao" sort="Yong, Xinhao" uniqKey="Yong X" first="Xinhao" last="Yong">Xinhao Yong</name></author><author><name sortKey="Zhu, Hong" sort="Zhu, Hong" uniqKey="Zhu H" first="Hong" last="Zhu">Hong Zhu</name></author><author><name sortKey="Lei, Ming" sort="Lei, Ming" uniqKey="Lei M" first="Ming" last="Lei">Ming Lei</name></author><author><name sortKey="Duan, Qing" sort="Duan, Qing" uniqKey="Duan Q" first="Qing" last="Duan">Qing Duan</name></author></analytic><series><title level="j">DNA and cell biology</title><idno type="ISSN">1044-5498</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, 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Infections</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en"><term>Reoviridae</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Reoviridae</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Fever</term><term>Lung</term><term>Lymph Nodes</term><term>Pulmonary Alveoli</term><term>Reoviridae Infections</term><term>Severe Acute Respiratory Syndrome</term><term>Spleen</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Chlorocebus aethiops</term><term>Disease Models, Animal</term><term>Female</term><term>Humans</term><term>Macaca</term><term>Male</term><term>Vero Cells</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Experimental studies were performed to determine the role of a newly isolated reovirus (ReoV) from a severe acute respiratory syndrome (SARS) patient in the etiology of this newly described serious respiratory syndrome. Four cynomologus macaques were inoculated with this reovirus (BYD1) in an attempt to replicate the infection and pathology observed in SARS. The body temperature of the infected monkeys was monitored three times a day, and blood and fecal samples were periodically collected for specific immunology determinations. On days 7 and 33 after inoculation, necropsies for pathological accessment and pathogen isolation were performed. The four infected macaques developed a fever on days 3 and 4 after inoculation, and maintainted a febrile state for 4-6 days. The highest temperature in the animals recorded was 40.4 degrees C. After a recovery phase, the macaques developed a second febrile condition. Antibody titers against the reovirus injected by the intravenous route occurred in higher number than those in the nasal cavity. Four macaque monkeys demonstrated diffuse alveolar damage, characterized by hemorrhagic pneumonia, serosanguineous exudates, formation of hyaline membranes, and type II pneumocyte hyperplasia, which were similar to those that have been noted in SARS patients. Lymphocytes decreased in the cortex of the lymph node and in the white pulp of the spleen. ReoV was detected in pneumonic tissue by virus isolation and RT-PCR. The macaques infected with the newly isolated reovirus developed a fever, diffuse alveolar damage and pulmonary interstitial inflammation similar to that noted in SARS patients. This evidence demonstrates that ReoV might have a primary role in the etiology of SARS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16101346</PMID><DateCompleted><Year>2005</Year><Month>09</Month><Day>29</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1044-5498</ISSN><JournalIssue CitedMedium="Print"><Volume>24</Volume><Issue>8</Issue><PubDate><Year>2005</Year><Month>Aug</Month></PubDate></JournalIssue><Title>DNA and cell biology</Title><ISOAbbreviation>DNA Cell Biol.</ISOAbbreviation></Journal><ArticleTitle>Experimental infection of macaques with the human reovirus BYD1 strain: an animal model for the study of the severe acute respiratory syndrome.</ArticleTitle><Pagination><MedlinePgn>491-5</MedlinePgn></Pagination><Abstract><AbstractText>Experimental studies were performed to determine the role of a newly isolated reovirus (ReoV) from a severe acute respiratory syndrome (SARS) patient in the etiology of this newly described serious respiratory syndrome. Four cynomologus macaques were inoculated with this reovirus (BYD1) in an attempt to replicate the infection and pathology observed in SARS. The body temperature of the infected monkeys was monitored three times a day, and blood and fecal samples were periodically collected for specific immunology determinations. On days 7 and 33 after inoculation, necropsies for pathological accessment and pathogen isolation were performed. The four infected macaques developed a fever on days 3 and 4 after inoculation, and maintainted a febrile state for 4-6 days. The highest temperature in the animals recorded was 40.4 degrees C. After a recovery phase, the macaques developed a second febrile condition. Antibody titers against the reovirus injected by the intravenous route occurred in higher number than those in the nasal cavity. Four macaque monkeys demonstrated diffuse alveolar damage, characterized by hemorrhagic pneumonia, serosanguineous exudates, formation of hyaline membranes, and type II pneumocyte hyperplasia, which were similar to those that have been noted in SARS patients. Lymphocytes decreased in the cortex of the lymph node and in the white pulp of the spleen. ReoV was detected in pneumonic tissue by virus isolation and RT-PCR. The macaques infected with the newly isolated reovirus developed a fever, diffuse alveolar damage and pulmonary interstitial inflammation similar to that noted in SARS patients. This evidence demonstrates that ReoV might have a primary role in the etiology of SARS.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>He</LastName><ForeName>Cheng</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Laboratory Animal Institute, College of Veterinary Medicine, China Agricultural University, Beijing, People's Republic of China. hecheng@cau.edu.cn</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pang</LastName><ForeName>Wanyong</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Yong</LastName><ForeName>Xinhao</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Hong</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Lei</LastName><ForeName>Ming</ForeName><Initials>M</Initials></Author><Author 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Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002522" MajorTopicYN="N">Chlorocebus aethiops</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="Y">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005334" MajorTopicYN="N">Fever</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008198" MajorTopicYN="N">Lymph Nodes</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008251" 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