Closely related influenza viruses induce contrasting respiratory tract immunopathology.
Identifieur interne : 000937 ( PubMed/Curation ); précédent : 000936; suivant : 000938Closely related influenza viruses induce contrasting respiratory tract immunopathology.
Auteurs : Vy L. Le [États-Unis] ; Cynthia L. Courtney ; John Steel ; Richard W. CompansSource :
- PloS one [ 1932-6203 ] ; 2013.
Descripteurs français
- KwdFr :
- Animaux, Antigènes viraux (métabolisme), Cellules myéloïdes (virologie), Cellules rénales canines Madin-Darby, Charge virale, Chiens, Chimiokines (métabolisme), Données de séquences moléculaires, Femelle, Maladies de l'appareil respiratoire (immunologie), Maladies de l'appareil respiratoire (métabolisme), Maladies de l'appareil respiratoire (virologie), Muqueuse respiratoire (immunologie), Muqueuse respiratoire (métabolisme), Muqueuse respiratoire (virologie), Réplication virale, Souris, Sous-type H1N1 du virus de la grippe A (), Sous-type H1N1 du virus de la grippe A (immunologie), Sous-type H1N1 du virus de la grippe A (pathogénicité), Sous-type H1N1 du virus de la grippe A (physiologie), Spécificité d'espèce, Séquence d'acides aminés.
- MESH :
- immunologie : Maladies de l'appareil respiratoire, Muqueuse respiratoire, Sous-type H1N1 du virus de la grippe A.
- métabolisme : Antigènes viraux, Chimiokines, Maladies de l'appareil respiratoire, Muqueuse respiratoire.
- pathogénicité : Sous-type H1N1 du virus de la grippe A.
- physiologie : Sous-type H1N1 du virus de la grippe A.
- virologie : Cellules myéloïdes, Maladies de l'appareil respiratoire, Muqueuse respiratoire.
- Animaux, Cellules rénales canines Madin-Darby, Charge virale, Chiens, Données de séquences moléculaires, Femelle, Réplication virale, Souris, Sous-type H1N1 du virus de la grippe A, Spécificité d'espèce, Séquence d'acides aminés.
English descriptors
- KwdEn :
- Amino Acid Sequence, Animals, Antigens, Viral (metabolism), Chemokines (metabolism), Dogs, Female, Influenza A Virus, H1N1 Subtype (classification), Influenza A Virus, H1N1 Subtype (immunology), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza A Virus, H1N1 Subtype (physiology), Madin Darby Canine Kidney Cells, Mice, Molecular Sequence Data, Myeloid Cells (virology), Respiratory Mucosa (immunology), Respiratory Mucosa (metabolism), Respiratory Mucosa (virology), Respiratory Tract Diseases (immunology), Respiratory Tract Diseases (metabolism), Respiratory Tract Diseases (virology), Species Specificity, Viral Load, Virus Replication.
- MESH :
- chemical , metabolism : Antigens, Viral, Chemokines.
- classification : Influenza A Virus, H1N1 Subtype.
- immunology : Influenza A Virus, H1N1 Subtype, Respiratory Mucosa, Respiratory Tract Diseases.
- metabolism : Respiratory Mucosa, Respiratory Tract Diseases.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- physiology : Influenza A Virus, H1N1 Subtype.
- virology : Myeloid Cells, Respiratory Mucosa, Respiratory Tract Diseases.
- Amino Acid Sequence, Animals, Dogs, Female, Madin Darby Canine Kidney Cells, Mice, Molecular Sequence Data, Species Specificity, Viral Load, Virus Replication.
Abstract
The swine-origin H1N1 virus which emerged in 2009 resulted in the first influenza pandemic of the 21(st) century. Although the majority of infections were moderate, a significant proportion of infections were severe and characterized by acute respiratory distress syndrome and pulmonary edema. We compared two isolates from the 2009 H1N1 pandemic; A/California/07/09 (CA/07) and A/Netherlands/602/09 (NL/602) viruses that share greater than 99% sequence identity. Though genetically similar, these viruses exhibit contrasting pathological effects. Mice that were infected with 800 plaque forming unit (PFU) of CA/07 virus rapidly lost weight, which was concurrent with detection of high pulmonary concentrations of MCP-1, MIG, IP-10 and TIMP-1. Initially, severe bronchiolar epithelial necrosis and acute respiratory distress was observed, followed by marked bronchiolar epithelial hyperplasia. Mononuclear cell infiltration was initially localized to perivascular and peribronchiolar interstitium and then spread to adjacent alveoli. Infiltrating cells were phenotypically CD11b(hi), F4/80(lo). In contrast, when mice were infected with 800 PFU of NL/602 virus, minimal weight loss was observed, and concentrations of cytokines in the lung were significantly lower. Inflammation was primarily restricted to the bronchioles and perivascular interstitium with minimal spread to alveoli. Infiltrating cells include foamy macrophages and surface markers were characterized as CD11b(lo/-), F4/80(hi). These two genetically similar viruses can be useful strains with which to investigate immune-regulatory determinants of pathogenesis of influenza virus.
DOI: 10.1371/journal.pone.0076708
PubMed: 24086762
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Although the majority of infections were moderate, a significant proportion of infections were severe and characterized by acute respiratory distress syndrome and pulmonary edema. We compared two isolates from the 2009 H1N1 pandemic; A/California/07/09 (CA/07) and A/Netherlands/602/09 (NL/602) viruses that share greater than 99% sequence identity. Though genetically similar, these viruses exhibit contrasting pathological effects. Mice that were infected with 800 plaque forming unit (PFU) of CA/07 virus rapidly lost weight, which was concurrent with detection of high pulmonary concentrations of MCP-1, MIG, IP-10 and TIMP-1. Initially, severe bronchiolar epithelial necrosis and acute respiratory distress was observed, followed by marked bronchiolar epithelial hyperplasia. Mononuclear cell infiltration was initially localized to perivascular and peribronchiolar interstitium and then spread to adjacent alveoli. Infiltrating cells were phenotypically CD11b(hi), F4/80(lo). In contrast, when mice were infected with 800 PFU of NL/602 virus, minimal weight loss was observed, and concentrations of cytokines in the lung were significantly lower. Inflammation was primarily restricted to the bronchioles and perivascular interstitium with minimal spread to alveoli. Infiltrating cells include foamy macrophages and surface markers were characterized as CD11b(lo/-), F4/80(hi). These two genetically similar viruses can be useful strains with which to investigate immune-regulatory determinants of pathogenesis of influenza virus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24086762</PMID><DateCompleted><Year>2014</Year><Month>06</Month><Day>16</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>9</Issue><PubDate><Year>2013</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Closely related influenza viruses induce contrasting respiratory tract immunopathology.</ArticleTitle><Pagination><MedlinePgn>e76708</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0076708</ELocationID><Abstract><AbstractText>The swine-origin H1N1 virus which emerged in 2009 resulted in the first influenza pandemic of the 21(st) century. Although the majority of infections were moderate, a significant proportion of infections were severe and characterized by acute respiratory distress syndrome and pulmonary edema. We compared two isolates from the 2009 H1N1 pandemic; A/California/07/09 (CA/07) and A/Netherlands/602/09 (NL/602) viruses that share greater than 99% sequence identity. Though genetically similar, these viruses exhibit contrasting pathological effects. Mice that were infected with 800 plaque forming unit (PFU) of CA/07 virus rapidly lost weight, which was concurrent with detection of high pulmonary concentrations of MCP-1, MIG, IP-10 and TIMP-1. Initially, severe bronchiolar epithelial necrosis and acute respiratory distress was observed, followed by marked bronchiolar epithelial hyperplasia. Mononuclear cell infiltration was initially localized to perivascular and peribronchiolar interstitium and then spread to adjacent alveoli. Infiltrating cells were phenotypically CD11b(hi), F4/80(lo). In contrast, when mice were infected with 800 PFU of NL/602 virus, minimal weight loss was observed, and concentrations of cytokines in the lung were significantly lower. Inflammation was primarily restricted to the bronchioles and perivascular interstitium with minimal spread to alveoli. Infiltrating cells include foamy macrophages and surface markers were characterized as CD11b(lo/-), F4/80(hi). These two genetically similar viruses can be useful strains with which to investigate immune-regulatory determinants of pathogenesis of influenza virus.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Le</LastName><ForeName>Vy L</ForeName><Initials>VL</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Courtney</LastName><ForeName>Cynthia L</ForeName><Initials>CL</Initials></Author><Author ValidYN="Y"><LastName>Steel</LastName><ForeName>John</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Compans</LastName><ForeName>Richard W</ForeName><Initials>RW</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI074579</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HHSN266200700006C</GrantID><Agency>PHS HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P51OD11132</GrantID><Acronym>OD</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32AI074492</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><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>2013</Year><Month>09</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000956">Antigens, Viral</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018925">Chemokines</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000595" MajorTopicYN="N">Amino Acid Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000956" MajorTopicYN="N">Antigens, Viral</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018925" MajorTopicYN="N">Chemokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName><QualifierName UI="Q000145" MajorTopicYN="N">classification</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061985" MajorTopicYN="N">Madin Darby Canine Kidney Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D022423" MajorTopicYN="N">Myeloid Cells</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020545" MajorTopicYN="N">Respiratory Mucosa</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012140" MajorTopicYN="N">Respiratory Tract Diseases</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013045" MajorTopicYN="N">Species Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019562" MajorTopicYN="N">Viral Load</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>06</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>08</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>10</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>10</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>6</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24086762</ArticleId><ArticleId 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