Deletions in the neuraminidase stalk region of H2N2 and H9N2 avian influenza virus subtypes do not affect postinfluenza secondary bacterial pneumonia.
Identifieur interne : 000152 ( PubMed/Corpus ); précédent : 000151; suivant : 000153Deletions in the neuraminidase stalk region of H2N2 and H9N2 avian influenza virus subtypes do not affect postinfluenza secondary bacterial pneumonia.
Auteurs : Ashok K. Chockalingam ; Danielle Hickman ; Lindomar Pena ; Jianqiang Ye ; Andrea Ferrero ; Jose R. Echenique ; Hongjun Chen ; Troy Sutton ; Daniel R. PerezSource :
- Journal of virology [ 1098-5514 ] ; 2012.
English descriptors
- KwdEn :
- Amino Acid Motifs, Animals, Bacterial Adhesion, Cell Line, Chickens, Coinfection (microbiology), Coinfection (virology), Female, Gene Deletion, Humans, Influenza A Virus, H2N2 Subtype (chemistry), Influenza A Virus, H2N2 Subtype (enzymology), Influenza A Virus, H2N2 Subtype (genetics), Influenza A Virus, H9N2 Subtype (chemistry), Influenza A Virus, H9N2 Subtype (enzymology), Influenza A Virus, H9N2 Subtype (genetics), Influenza in Birds (virology), Influenza, Human (complications), Influenza, Human (virology), Lung (microbiology), Lung (virology), Mice, Mice, Inbred BALB C, Neuraminidase (chemistry), Neuraminidase (genetics), Neuraminidase (metabolism), Pneumonia, Bacterial (complications), Pneumonia, Bacterial (microbiology), Streptococcus pneumoniae (physiology), Viral Proteins (chemistry), Viral Proteins (genetics), Viral Proteins (metabolism).
- MESH :
- chemical , chemistry : Neuraminidase, Viral Proteins.
- chemistry : Influenza A Virus, H2N2 Subtype, Influenza A Virus, H9N2 Subtype.
- complications : Influenza, Human, Pneumonia, Bacterial.
- enzymology : Influenza A Virus, H2N2 Subtype, Influenza A Virus, H9N2 Subtype.
- genetics : Influenza A Virus, H2N2 Subtype, Influenza A Virus, H9N2 Subtype, Neuraminidase, Viral Proteins.
- chemical , metabolism : Neuraminidase, Viral Proteins.
- microbiology : Coinfection, Lung, Pneumonia, Bacterial.
- physiology : Streptococcus pneumoniae.
- virology : Coinfection, Influenza in Birds, Influenza, Human, Lung.
- Amino Acid Motifs, Animals, Bacterial Adhesion, Cell Line, Chickens, Female, Gene Deletion, Humans, Mice, Mice, Inbred BALB C.
Abstract
We investigated the synergism between influenza virus and Streptococcus pneumoniae, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of S. pneumoniae to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential S. pneumoniae infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with S. pneumoniae. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.
DOI: 10.1128/JVI.05809-11
PubMed: 22278240
Links to Exploration step
pubmed:22278240Le document en format XML
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Chockalingam</name><affiliation><nlm:affiliation>Department of Veterinary Medicine, University of Maryland, College Park, Maryland, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Hickman, Danielle" sort="Hickman, Danielle" uniqKey="Hickman D" first="Danielle" last="Hickman">Danielle Hickman</name></author><author><name sortKey="Pena, Lindomar" sort="Pena, Lindomar" uniqKey="Pena L" first="Lindomar" last="Pena">Lindomar Pena</name></author><author><name sortKey="Ye, Jianqiang" sort="Ye, Jianqiang" uniqKey="Ye J" first="Jianqiang" last="Ye">Jianqiang Ye</name></author><author><name sortKey="Ferrero, Andrea" sort="Ferrero, Andrea" uniqKey="Ferrero A" first="Andrea" last="Ferrero">Andrea Ferrero</name></author><author><name sortKey="Echenique, Jose R" sort="Echenique, Jose R" uniqKey="Echenique J" first="Jose R" last="Echenique">Jose R. 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Echenique</name></author><author><name sortKey="Chen, Hongjun" sort="Chen, Hongjun" uniqKey="Chen H" first="Hongjun" last="Chen">Hongjun Chen</name></author><author><name sortKey="Sutton, Troy" sort="Sutton, Troy" uniqKey="Sutton T" first="Troy" last="Sutton">Troy Sutton</name></author><author><name sortKey="Perez, Daniel R" sort="Perez, Daniel R" uniqKey="Perez D" first="Daniel R" last="Perez">Daniel R. Perez</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Motifs</term><term>Animals</term><term>Bacterial Adhesion</term><term>Cell Line</term><term>Chickens</term><term>Coinfection (microbiology)</term><term>Coinfection (virology)</term><term>Female</term><term>Gene Deletion</term><term>Humans</term><term>Influenza A Virus, H2N2 Subtype (chemistry)</term><term>Influenza A Virus, H2N2 Subtype (enzymology)</term><term>Influenza A Virus, H2N2 Subtype (genetics)</term><term>Influenza A Virus, H9N2 Subtype (chemistry)</term><term>Influenza A Virus, H9N2 Subtype (enzymology)</term><term>Influenza A Virus, H9N2 Subtype (genetics)</term><term>Influenza in Birds (virology)</term><term>Influenza, Human (complications)</term><term>Influenza, Human (virology)</term><term>Lung (microbiology)</term><term>Lung (virology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Neuraminidase (chemistry)</term><term>Neuraminidase (genetics)</term><term>Neuraminidase (metabolism)</term><term>Pneumonia, Bacterial (complications)</term><term>Pneumonia, Bacterial (microbiology)</term><term>Streptococcus pneumoniae (physiology)</term><term>Viral Proteins (chemistry)</term><term>Viral Proteins (genetics)</term><term>Viral Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Neuraminidase</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Influenza A Virus, H2N2 Subtype</term><term>Influenza A Virus, H9N2 Subtype</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Influenza, Human</term><term>Pneumonia, Bacterial</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Influenza A Virus, H2N2 Subtype</term><term>Influenza A Virus, H9N2 Subtype</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A Virus, H2N2 Subtype</term><term>Influenza A Virus, H9N2 Subtype</term><term>Neuraminidase</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Neuraminidase</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Coinfection</term><term>Lung</term><term>Pneumonia, Bacterial</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Streptococcus pneumoniae</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coinfection</term><term>Influenza in Birds</term><term>Influenza, Human</term><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Motifs</term><term>Animals</term><term>Bacterial Adhesion</term><term>Cell Line</term><term>Chickens</term><term>Female</term><term>Gene Deletion</term><term>Humans</term><term>Mice</term><term>Mice, Inbred BALB C</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated the synergism between influenza virus and Streptococcus pneumoniae, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of S. pneumoniae to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential S. pneumoniae infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with S. pneumoniae. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22278240</PMID><DateCompleted><Year>2012</Year><Month>06</Month><Day>11</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>86</Volume><Issue>7</Issue><PubDate><Year>2012</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Deletions in the neuraminidase stalk region of H2N2 and H9N2 avian influenza virus subtypes do not affect postinfluenza secondary bacterial pneumonia.</ArticleTitle><Pagination><MedlinePgn>3564-73</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.05809-11</ELocationID><Abstract><AbstractText>We investigated the synergism between influenza virus and Streptococcus pneumoniae, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of S. pneumoniae to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential S. pneumoniae infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with S. pneumoniae. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chockalingam</LastName><ForeName>Ashok K</ForeName><Initials>AK</Initials><AffiliationInfo><Affiliation>Department of Veterinary Medicine, University of Maryland, College Park, Maryland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hickman</LastName><ForeName>Danielle</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Pena</LastName><ForeName>Lindomar</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Ye</LastName><ForeName>Jianqiang</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Ferrero</LastName><ForeName>Andrea</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Echenique</LastName><ForeName>Jose R</ForeName><Initials>JR</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Hongjun</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Sutton</LastName><ForeName>Troy</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Perez</LastName><ForeName>Daniel R</ForeName><Initials>DR</Initials></Author></AuthorList><Language>eng</Language><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>2012</Year><Month>01</Month><Day>25</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="D014764">Viral Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.2.1.18</RegistryNumber><NameOfSubstance UI="C487630">NA protein, influenza A virus</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.2.1.18</RegistryNumber><NameOfSubstance UI="D009439">Neuraminidase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D020816" MajorTopicYN="N">Amino Acid Motifs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001422" MajorTopicYN="N">Bacterial Adhesion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell 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MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053127" MajorTopicYN="N">Influenza A Virus, H9N2 Subtype</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005585" MajorTopicYN="N">Influenza in Birds</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</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="D009439" MajorTopicYN="N">Neuraminidase</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018410" MajorTopicYN="N">Pneumonia, Bacterial</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013296" MajorTopicYN="N">Streptococcus pneumoniae</DescriptorName><QualifierName UI="Q000502" 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|étape= Corpus
|type= RBID
|clé= pubmed:22278240
|texte= Deletions in the neuraminidase stalk region of H2N2 and H9N2 avian influenza virus subtypes do not affect postinfluenza secondary bacterial pneumonia.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:22278240" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a H2N2V1
| This area was generated with Dilib version V0.6.33. |  |